33.3: Homeostasis - Biology

33.3: Homeostasis - Biology

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33.3: Homeostasis


Homeostasis is an organism’s process of maintaining a stable internal environment suitable for sustaining life. The word homeostasis derives from Greek, with home meaning “similar,” and stasis, meaning “stable.” When used as an adjective, it is homeostatic.

We normally think about homeostasis in terms of the whole body, but individual systems – that is, groups of organs – also maintain homeostatic conditions. Nonetheless, prolonged imbalance in just one system can negatively impact the homeostasis of the entire organism.

33.3 Antibodies

In this section, you will explore the following questions:

  • What is cross-reactivity?
  • What is the basic structure of an antibody, and what are the functions of antibodies?
  • How are antibodies produced?

Connection for AP ® Courses

Much of the information in this section is not within the scope for AP ® . Antibodies, also known as immunoglobulins, are proteins produced and secreted by plasma cells (differentiated B lymphocytes) that mediate the humoral immune response. Antibodies are Y-shaped proteins consisting of four polypeptides with at least two binding sites for a specific antigen. The areas where the antigen is recognized on the antibody are variable domains. For AP ® , you do not need to know the different classes of antibodies or the molecular structure of a specific antibody. What is important to understand is that antibodies are antigen-specific. When antibodies bind antigens, they can neutralize pathogens, mark them for phagocytosis, or activate the complement cascade. Because secreted antibodies can remain in the circulation for many years, secondary exposure to a pathogen results in a faster immune response. Antibodies occur in the blood, in gastric and mucus secretions, and in breast milk, thus providing passive immunity to the infant.

Information presented and the examples highlighted in the section support concepts outlined in Big Idea 2 and Big Idea 4 of the AP ® Biology Curriculum Framework. The AP ® Learning Objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

Big Idea 2 Biological systems utilize free energy and molecular building blocks to grow, to reproduce, and to maintain dynamic homeostasis.
Enduring Understanding 2.D Growth and dynamic homeostasis of a biological system are influenced by changes in the system’s environment.
Essential Knowledge 2.D.4 Plants and animals have a variety of chemical defenses against infections that affect dynamic homeostasis.
Science Practice 1.1 The student can create representations and models of natural or man-made phenomena and systems in the domain.
Science Practice 1.2 The student can describe representations and models of natural or man-made phenomena and systems in the domain.
Learning Objective 2.30 The student can create representations or models to describe nonspecific immune defenses in animals.
Big Idea 4 Biological systems interact, and these systems and their interactions possess complex properties.
Enduring Understanding 4.C Naturally occurring diversity among and between components within biological systems affects interactions with the environment.
Essential Knowledge 4.C.1 Variation in molecular units provides cells with a wider range of functions.
Science Practice 6.2 The student can construct explanations of phenomena based on evidence produced through scientific practices.
Learning Objective 4.22 The student is able to construct explanations based on evidence of how variation in molecular units provides cells with a wider range of functions.

Antibody Structure

An antibody molecule is comprised of four polypeptides: two identical heavy chains (large peptide units) that are partially bound to each other in a “Y” formation, which are flanked by two identical light chains (small peptide units), as illustrated in Figure 33.22. Bonds between the cysteine amino acids in the antibody molecule attach the polypeptides to each other. The areas where the antigen is recognized on the antibody are variable domains and the antibody base is composed of constant domains.

In germ-line B cells, the variable region of the light chain gene has 40 variable (V) and five joining (J) segments. An enzyme called DNA recombinase randomly excises most of these segments out of the gene, and splices one V segment to one J segment. During RNA processing, all but one V and J segment are spliced out. Recombination and splicing may result in over 10 6 possible VJ combinations. As a result, each differentiated B cell in the human body typically has a unique variable chain. The constant domain, which does not bind antibody, is the same for all antibodies.

Similar to TCRs and BCRs, antibody diversity is produced by the mutation and recombination of approximately 300 different gene segments encoding the light and heavy chain variable domains in precursor cells that are destined to become B cells. The variable domains from the heavy and light chains interact to form the binding site through which an antibody can bind a specific epitope on an antigen. The numbers of repeated constant domains in Ig classes are the same for all antibodies corresponding to a specific class. Antibodies are structurally similar to the extracellular component of the BCRs, and B cell maturation to plasma cells can be visualized in simple terms as the cell acquires the ability to secrete the extracellular portion of its BCR in large quantities.

Antibody Classes

Antibodies can be divided into five classes—IgM, IgG, IgA, IgD, IgE—based on their physiochemical, structural, and immunological properties. IgGs, which make up about 80 percent of all antibodies, have heavy chains that consist of one variable domain and three identical constant domains. IgA and IgD also have three constant domains per heavy chain, whereas IgM and IgE each have four constant domains per heavy chain. The variable domain determines binding specificity and the constant domain of the heavy chain determines the immunological mechanism of action of the corresponding antibody class. It is possible for two antibodies to have the same binding specificities but be in different classes and, therefore, to be involved in different functions.

After an adaptive defense is produced against a pathogen, typically plasma cells first secrete IgM into the blood. BCRs on naïve B cells are of the IgM class and occasionally IgD class. IgM molecules make up approximately ten percent of all antibodies. Prior to antibody secretion, plasma cells assemble IgM molecules into pentamers (five individual antibodies) linked by a joining (J) chain, as shown in Figure 33.23. The pentamer arrangement means that these macromolecules can bind ten identical antigens. However, IgM molecules released early in the adaptive immune response do not bind to antigens as stably as IgGs, which are one of the possible types of antibodies secreted in large quantities upon re-exposure to the same pathogen. Figure 33.23 summarizes the properties of immunoglobulins and illustrates their basic structures.

IgAs populate the saliva, tears, breast milk, and mucus secretions of the gastrointestinal, respiratory, and genitourinary tracts. Collectively, these bodily fluids coat and protect the extensive mucosa (4000 square feet in humans). The total number of IgA molecules in these bodily secretions is greater than the number of IgG molecules in the blood serum. A small amount of IgA is also secreted into the serum in monomeric form. Conversely, some IgM is secreted into bodily fluids of the mucosa. Similar to IgM, IgA molecules are secreted as polymeric structures linked with a J chain. However, IgAs are secreted mostly as dimeric molecules, not pentamers.

IgE is present in the serum in small quantities and is best characterized in its role as an allergy mediator. IgD is also present in small quantities. Similar to IgM, BCRs of the IgD class are found on the surface of naïve B cells. This class supports antigen recognition and maturation of B cells to plasma cells.

Antibody Functions

Differentiated plasma cells are crucial players in the humoral response, and the antibodies they secrete are particularly significant against extracellular pathogens and toxins. Antibodies circulate freely and act independently of plasma cells. Antibodies can be transferred from one individual to another to temporarily protect against infectious disease. For instance, a person who has recently produced a successful immune response against a particular disease agent can donate blood to a nonimmune recipient and confer temporary immunity through antibodies in the donor’s blood serum. This phenomenon is called passive immunity it also occurs naturally during breastfeeding, which makes breastfed infants highly resistant to infections during the first few months of life.

Antibodies coat extracellular pathogens and neutralize them, as illustrated in Figure 33.24, by blocking key sites on the pathogen that enhance their infectivity (such as receptors that “dock” pathogens on host cells). Antibody neutralization can prevent pathogens from entering and infecting host cells, as opposed to the CTL-mediated approach of killing cells that are already infected to prevent progression of an established infection. The neutralized antibody-coated pathogens can then be filtered by the spleen and eliminated in urine or feces.

Antibodies also mark pathogens for destruction by phagocytic cells, such as macrophages or neutrophils, because phagocytic cells are highly attracted to macromolecules complexed with antibodies. Phagocytic enhancement by antibodies is called opsonization. In a process called complement fixation, IgM and IgG in serum bind to antigens and provide docking sites onto which sequential complement proteins can bind. The combination of antibodies and complement enhances opsonization even further and promotes rapid clearing of pathogens.

Affinity, Avidity, and Cross Reactivity

Not all antibodies bind with the same strength, specificity, and stability. In fact, antibodies exhibit different affinities (attraction) depending on the molecular complementarity between antigen and antibody molecules, as illustrated in Figure 33.25. An antibody with a higher affinity for a particular antigen would bind more strongly and stably, and thus would be expected to present a more challenging defense against the pathogen corresponding to the specific antigen.

The term avidity describes binding by antibody classes that are secreted as joined, multivalent structures (such as IgM and IgA). Although avidity measures the strength of binding, just as affinity does, the avidity is not simply the sum of the affinities of the antibodies in a multimeric structure. The avidity depends on the number of identical binding sites on the antigen being detected, as well as other physical and chemical factors. Typically, multimeric antibodies, such as pentameric IgM, are classified as having lower affinity than monomeric antibodies, but high avidity. Essentially, the fact that multimeric antibodies can bind many antigens simultaneously balances their slightly lower binding strength for each antibody/antigen interaction.

Antibodies secreted after binding to one epitope on an antigen may exhibit cross reactivity for the same or similar epitopes on different antigens. Because an epitope corresponds to such a small region (the surface area of about four to six amino acids), it is possible for different macromolecules to exhibit the same molecular identities and orientations over short regions. Cross reactivity describes when an antibody binds not to the antigen that elicited its synthesis and secretion, but to a different antigen.

Cross reactivity can be beneficial if an individual develops immunity to several related pathogens despite having only been exposed to or vaccinated against one of them. For instance, antibody cross reactivity may occur against the similar surface structures of various Gram-negative bacteria. Conversely, antibodies raised against pathogenic molecular components that resemble self molecules may incorrectly mark host cells for destruction and cause autoimmune damage. Patients who develop systemic lupus erythematosus (SLE) commonly exhibit antibodies that react with their own DNA. These antibodies may have been initially raised against the nucleic acid of microorganisms but later cross-reacted with self-antigens. This phenomenon is also called molecular mimicry.

Antibodies of the Mucosal Immune System

Antibodies synthesized by the mucosal immune system include IgA and IgM. Activated B cells differentiate into mucosal plasma cells that synthesize and secrete dimeric IgA, and to a lesser extent, pentameric IgM. Secreted IgA is abundant in tears, saliva, breast milk, and in secretions of the gastrointestinal and respiratory tracts. Antibody secretion results in a local humoral response at epithelial surfaces and prevents infection of the mucosa by binding and neutralizing pathogens.

33.3: Homeostasis - Biology

Chapter 33
Comparing Chordates

In this chapter, students will read about broad trends in the evolution of the chordates and compare the adaptations of the major living groups of chordates.The links below lead to additional resources to help you with this chapter. These include Hot Links to Web sites related to the topics in this chapter, the Take It to the Net activities referred to in your textbook, a Self-Test you can use to test your knowledge of this chapter, and Teaching Links that instructors may find useful for their students.

Section 33-1: Chordate Evolution
The chordate family tree has its roots in ancestors that vertebrates share with tunicates and lancelets.
Over the course of evolution, the appearance of new adaptations—such as jaws and paired appendages—has launched adaptive radiation in chordate groups.

Section 33-2: Controlling Body Temperature
The control of body temperature is important for maintaining homeostasis in many vertebrates, particularly in habitats where temperature varies widely with time of day and with season.
Most fishes, amphibians, and reptiles are ectotherms—organisms that obtain heat from outside their bodies. Birds and mammals are endotherms, which means they can generate heat inside their bodies.

Section 33-3: Form and Function in Chordates
The digestive systems of vertebrates have organs that are well adapted for different feeding habits.
Aquatic chordates—such as tunicates, fishes, and amphibian larvae—use gills for respiration. Land vertebrates, including adult amphibians, reptiles, birds, and mammals, use lungs.
During the course of chordate evolution, the heart developed chambers and partitions that help separate the blood traveling in the circulatory system.
Nonvertebrate chordates have a relatively simple nervous system with a mass of nerve cells that form a brain. Vertebrates have a more complex brain with distinct regions, each with a different function.
Muscular and skeletal systems support a vertebrate's body and make it possible to control movement.

Definition of Homeostasis

Homeostasis: A property of cells, tissues, and organisms that allows the maintenance and regulation of the stability and constancy needed to function properly. Homeostasis is a healthy state that is maintained by the constant adjustment of biochemical and physiological pathways. An example of homeostasis is the maintenance of a constant blood pressure in the human body through a series of fine adjustments in the normal range of function of the hormonal, neuromuscular, and cardiovascular systems. These adjustments allow the maintenance of blood pressure needed for body function despite environmental changes and changes in a person's activity level and position. Other homeostatic mechanisms, for example, permit the maintenance of body temperature within a narrow range.


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Control of homeostasis

When a change occurs in an animal&rsquos environment, an adjustment must be made. The receptor senses the change in the environment, then sends a signal to the control center (in most cases, the brain) which in turn generates a response that is signaled to an effector. The effector is a muscle (that contracts or relaxes) or a gland that secretes. Homeostatsis is maintained by negative feedback loops. Positive feedback loops actually push the organism further out of homeostasis, but may be necessary for life to occur. Homeostasis is controlled by the nervous and endocrine system of mammals.

A physiologist's view of homeostasis

Homeostasis is a core concept necessary for understanding the many regulatory mechanisms in physiology. Claude Bernard originally proposed the concept of the constancy of the “milieu interieur,” but his discussion was rather abstract. Walter Cannon introduced the term “homeostasis” and expanded Bernard's notion of 𠇌onstancy” of the internal environment in an explicit and concrete way. In the 1960s, homeostatic regulatory mechanisms in physiology began to be described as discrete processes following the application of engineering control system analysis to physiological systems. Unfortunately, many undergraduate texts continue to highlight abstract aspects of the concept rather than emphasizing a general model that can be specifically and comprehensively applied to all homeostatic mechanisms. As a result, students and instructors alike often fail to develop a clear, concise model with which to think about such systems. In this article, we present a standard model for homeostatic mechanisms to be used at the undergraduate level. We discuss common sources of confusion (“sticky points”) that arise from inconsistencies in vocabulary and illustrations found in popular undergraduate texts. Finally, we propose a simplified model and vocabulary set for helping undergraduate students build effective mental models of homeostatic regulation in physiological systems.

in 2007, a group of 21 biologists from a wide range of disciplines agreed that “homeostasis” was one of eight core concepts in biology (14). Two years later, the American Association of Medical Colleges and Howard Hughes Medical Institute in its report (1) on the scientific foundations for future physicians similarly identified the ability to apply knowledge about “homeostasis” as one of the core competencies (competency M1).

From our perspective as physiologists, it is clear that homeostasis is a core concept of our discipline. When we asked physiology instructors from a broad range of educational institutions what they thought the 𠇋ig ideas” (concepts) of physiology were, we found that they too identified “homeostasis” and �ll membranes” as the two most important big ideas in physiology (15). In a subsequent survey (16), physiology instructors ranked homeostasis as one of the core concepts critical to understanding physiology.

If, as these surveys indicate, the concept of homeostasis is central to understanding physiological mechanisms, one would expect that instructors and textbooks would present a consistent model of the concept. However, an examination of 11 commonly used undergraduate physiology and biology textbooks revealed that this is not necessarily the case (17). Explanations of the concept of homeostasis and subsequent references to the concept suffer from a number of shortcomings. Although these texts define some terms related to homeostatic regulatory systems, many authors do not use these terms consistently. Moreover, they do not always use consistent visual representations of the concept. In addition, the explanation of the concept often conflicts with the current understanding of homeostatic regulatory mechanisms. These limitations of textbooks most likely carry over to classroom instruction, thereby weakening the power of the concept as a unifying idea for understanding physiology.

The goals of this article are to develop a correct description and visual representation of a general homeostatic mechanism that can serve as a learning tool for faculty members and students. We will limit our discussion to homeostatic mechanisms found in organismal systems that maintain a constant extracellular compartment and will not consider other types of homeostasis. Although this tool can be useful at any academic level, our primary focus is its application at the undergraduate level when students are first introduced to the concept. We will also briefly discuss the history of the concept and then address the “sticky points” that may lead to confusion for faculty members and students alike when attempting to apply the concept to mammalian, organismal physiology. We conclude with suggestions for improving instruction on homeostasis and its applications.

History of the Concept of Homeostasis

Claude Bernard asserted that complex organisms are able to maintain their internal environment [extracellular fluid (ECF)] fairly constant in the face of challenges from the external world (8). He went on to say that 𠇊 free and independent existence is possible only because of the stability of the internal milieu” (3). Walter Cannon coined the term “homeostasis” with the intent of providing a term that would convey the general idea proposed some 50 yr earlier by Bernard (8). Cannon's view focused on maintaining a steady state within an organism regardless of whether the mechanisms involved were passive (e.g., water movement between capillaries and the interstitium reflecting a balance between hydrostatic and osmotic forces) or active (e.g., storage and release of intracellular glucose) (6). While we recognize the validity of both passive and active mechanisms of homeostasis, our consideration will focus exclusively on the active regulatory processes involved in maintaining homeostasis.

Early physiology textbooks reflected this broad definition by briefly mentioning Bernard's concept of the constancy of the internal milieu, but the term “homeostasis” was not used in discussions of specific regulatory mechanisms (9, 11, 4).

This situation began to change in the mid-1960s, when a branch of biomedical engineering emerged that focused on applying engineering control systems analysis to physiological systems (18, 19, 2, 20). Arthur Guyton was the first major physiology textbook author to include a control systems theory approach in his textbook, and his book included detailed attention to the body's many regulatory mechanisms (10). Hence, Guyton introduced many students to the concept of homeostasis as an active regulatory mechanism that tended to minimize disturbances to the internal environment.

Engineering control systems theory describes a variety of other mechanisms to maintain the stability of a system. Although many of these mechanisms may be found in biological systems (7), not all of them are components of homeostatic mechanisms. For instance, the ballistic system used by the nervous system for throwing a ball simply calculates in advance the pattern of commands needed to achieve some particular outcome based on previous experience (7). Here, there is no element involved that regulates the internal environment.

Homeostatic mechanisms originated to keep a regulated variable in the internal environment within a range of values compatible with life and, as has been more recently suggested, to reduce noise during information transfer in physiological systems (22). To emphasize the stabilizing process, we distinguish between a “regulated (sensed) variable” and a “nonregulated (controlled) variable” (5, 23). A regulated (sensed) variable is one for which a sensor exists within the system and that is kept within a limited range by physiological mechanisms (5). For example, blood pressure and body temperature are sensed variables. Baroreceptors and thermoreceptors exist within the system and provide the value of the pressure or temperature to the regulatory mechanism. We call variables that can be changed by the system, but for which sensors do not exist within the system, nonregulated (controlled) variables. Nonregulated variables are manipulated or modulated to achieve regulation of the variable being held constant. For example, heart rate can be changed by the autonomic nervous system to regulate blood pressure, but there are no sensors in the system that measure heart rate directly. Hence, heart rate is a nonregulated variable.

A simple model illustrating the fundamental engineering control system concepts relevant to homeostatic regulatory mechanisms is shown in Fig. 1 .

Diagram of a generic homeostatic regulatory system. If the value of the regulated variable is disturbed, this system functions to restore it toward its set point value and, hence, is also referred to as a negative feedback system.

This model, some version of which appears in many current physiology texts, includes the following five critical components that a regulatory system must contain to maintain homeostasis:

1. It must contain a sensor that measures the value of the regulated variable.

2. It must contain a mechanism for establishing the “normal range” of values for the regulated variable. In the model shown in Fig. 1 , this mechanism is represented by the “set point,” although this term is not meant to imply that this normal range is actually a “point” or that it has a fixed value. In the next section, we further discuss the notion of a set point.

3. It must contain an 𠇎rror detector” that compares the signal being transmitted by the sensor (representing the actual value of the regulated variable) with the set point. The result of this comparison is an error signal that is interpreted by the controller.

4. The controller interprets the error signal and determines the value of the outputs of the effectors.

5. The effectors are those elements that determine the value of the regulated variable.

Such a system operates in way that causes any change to the regulated variable, a disturbance, to be countered by a change in the effector output to restore the regulated variable toward its set point value. Systems that behave in this way are said to be negative feedback systems.

While the model shown in Fig. 1 is a relatively simple one, there is a great deal of information that can be packed into each of the boxes that constitute the model. Homeostasis can also be described as a hierarchically arranged set of statements, a conceptual framework, that contains whatever breath and depth of information is appropriate for a particular set of students in a course. We have developed and described such an “unpacking” of the core concept of homeostasis (12, 13). The model and the conceptual framework provide students with different tools for thinking about homeostasis.

Topics That Cause Confusion for Students and Instructors: Sticky Points

A sticky point is any conceptual difficulty that makes one's mental model of any phenomenon inaccurate and, hence, less useful. There are a number of factors that contribute to the generation of sticky points for both instructors and students:

The phenomenon in question is a complex one.

There are aspects of the phenomenon that are counterintuitive.

The language or terminology used to describe the phenomenon or concept is inconsistent.

The discipline's understanding of the phenomenon is uncertain or incomplete.

In this section, we will describe some sticky points about homeostatic regulatory mechanisms that we have uncovered as we have interacted with instructors and students about their understanding of homeostasis. We will address these sticky points in the form of a series of questions and answers.

What environment is regulated by organismal homeostasis?

Organismal homeostasis, as originally defined by Cannon (6), refers to physiological mechanisms that maintain relatively constant the variables related to the internal milieu of the organism. This includes variables related to the entire ECF compartment or to its subcompartments (e.g., the plasma). We will not be discussing intracellular homeostatic mechanisms.

Are all negative feedback systems homeostatic?

Although negative feedback is an essential element of homeostatic regulatory mechanisms, the presence of negative feedback in a system does not mean that the system is homeostatic in function. Negative feedback exists in many systems that do not involve homeostatic regulation. For example, negative feedback plays a role in the muscle stretch reflex, but this reflex is not involved with maintaining the constancy of the internal environment. In other cases, the presence of negative feedback may minimize oscillation of a variable, even though that variable itself is not maintained relatively constant (i.e., it is not a regulated variable). Control of the blood levels of cortisol is an example of the oscillating damping effects of negative feedback (see further discussion below).

Can other types of control mechanisms (e.g., feedforward) maintain homeostasis?

Feedforward or anticipatory control mechanisms permit the body to predict a change in the physiology of the organism and initiate a response that can reduce the movement of a regulated variable out of its normal range (7, 23). Thus, feedforward mechanisms may help minimize the effects of a perturbation and can help maintain homeostasis. For example, anticipatory increases in breathing frequency will reduce the time course of the response to exercise-induced hypoxia. Because of this, attempts have been made to broaden the definition of homeostasis to include a range of anticipatory mechanisms (23).

However, we have decided to limit our generic model of a homeostatic regulatory system ( Fig. 1 ) to one that illustrates negative feedback and demonstrates the minimization of an error signal. We have done this because our model is intended to help faculty members teach and students learn the core concept of homeostasis in introductory physiology (12, 13). There are additional complex features found in feedback systems that are not included here because our intention is to first help students make sense of the foundational concept of homeostatic regulation. As situations are encountered where this basic model is no longer adequate to predict system behavior (7, 23), additional elements like feedforward mechanisms can be added to the model.

What is a set point?

Understanding the concept of a set point is central to understanding the function of a homeostatic mechanism. The set point in an engineering control system is easily defined and understood it is the value of the regulated variable that the designer or operator of the system wants as the output of the system. The cruise control mechanism in an automobile is an example of a system with an easy to understand set point. The driver determines the desired speed for the car (the set point). The regulatory mechanism uses available effectors (the throttle actuators) and a negative feedback system to hold the speed constant in the face of changes in terrain and wind conditions. In such a system, we can envision an electronic circuit located in the engine control module that compares the actual ground speed with the set speed programmed by the driver and uses the error signal to control the throttle actuator appropriately.

In physiological systems, the set point is conceptually similar. However, one source of difficulty is that, in most cases, we do not know the molecular or cellular mechanisms that generate a signal of a particular magnitude. What is clear is that certain physiological systems behave as though there is a set point signal that is used to regulate a physiological variable (23).

Another challenge to our understanding of set points arises from the fact that set points are clearly changeable, either physiologically or as the result of a pathological change in the system (23). The mechanisms that cause variations in a set point can operate temporarily, permanently, or cyclically. Physiologically, this can occur as a result of discrete physiological phenomena (e.g., fever), the operation of hierarchical homeostats (e.g., regulation of ECF P co 2) (see Ref. 7), or through the influence of biological clocks (e.g., circadian or diurnal rhythms of body temperature). The observation that set points can be changed adds complexity to our understanding of homeostatic regulation and can lead to confusion about whether the measured change in a regulated variable results from a change in the physiological stimulus or from a changing set point (23). In these cases, it is important to make such distinctions between a change in the stimulus and the modulation of the set point to arrive at an accurate picture of how a particular homeostatically regulated system operates.

Do homeostatic mechanisms operate like an on/off switch?

Control signals are ALWAYS present, and they continuously determine the output of the effectors. Changes in the control signals alter effector outputs and therefore change the regulated variable. The amplitude of these control signals vary when there is an error signal (i.e., when the regulated variable is not the same as the set point). Thus, homeostatic regulation is a constant, continuous process and does not ordinarily operate as an on/off switch that results in an all-or-none response.

What is the difference between an effector and a physiological response?

Textbook diagrams and narratives can blur the distinction between the effector and a response generated by the effector, making it difficult for students to build a correct mental model. This problem can occur if, when a visual representation of a homeostatic mechanism is presented (see Fig. 1 ), a physiological response is placed in the same 𠇌oncept” box as the effector. For example, “increased secretion by sweat glands” and “vasodilation of blood vessels in the skin” might be identified as effectors in the control system for thermoregulation. However, only “sweat glands” and 𠇋lood vessels” are effectors, whereas “increased secretion” and “vasodilation” are the responses of the effectors. Comprehensive understanding of homeostatic mechanisms requires that we, and students, make clear distinctions between effectors and responses. The term �tor” should only be applied to a physical entity such as a cell, tissue, or organ, whereas responses such as secretion and vasodilation are actions, not physical entities.

Students may also be confused if only the change in the regulated variable is thought of as being the response of the effector. The change in the regulated variable is typically a consequence of changes in function caused by effectors that determine the value of the regulated variable. By applying the term “response” to only the change in the regulated variable, the intermediary steps between the action of the effector and the change in the regulated variable are not acknowledged explicitly. Under these circumstances, it would reasonable for students to conclude that the intermediary steps are, in some way, aspects of the effector rather than the effect of actions of the effectors. This practice may also reflect a lack of understanding of the difference between the regulated variable, e.g., body temperature, and all of the nonregulated variables that are modified (e.g., arteriole diameter and rate of sweat production) in the steps between the action of the effector and the change in the regulated variable.

What does “relatively constant over time” mean?

In the above sections, we emphasized that homeostatic mechanisms operate to keep a regulated variable in the internal environment “relatively constant.” This is a common phrase used to describe what normally happens to the value of the regulated variable over time. A potential sticky point arises from the use of this phrase. How much change can occur to a regulated variable that is held relatively constant? Three points of clarification need to be made. By saying relatively constant, we mean that:

1. Regulated variables are held within a narrower range of values than if they were not regulated.

2. The regulated value is maintained within a range that is consistent with the viability of the organism.

3. There are differences in the range of values permitted for different regulated variables.

The second point is key to understanding the range over which regulated variables can change homeostatic mechanisms operate to prevent a potentially lethal change in the internal environment. Indeed, as it is often used, relatively constant essentially serves as a surrogate phrase for within the range compatible with an organism's viability. For some regulated variables, the range is quite narrow (e.g., extracellular H + concentration or extracellular osmolarity). For other variables, the range can be broad under some circumstances (e.g., blood glucose concentration during the fed state) and narrow in other situations (e.g., blood glucose during the fasting state). The factors that contribute to the normal range or, in our model, the set point, of a particular variable are undoubtedly complex and, in most cases, have not been elucidated.

What physiological variables are homeostatically regulated?

To identify specific variables that may be homeostatically regulated, the five critical components illustrated in the model shown in Fig. 1 must be present. That is, a regulatory system for that variable must exist that contains the five critical components described in Fig. 1 . Based on this test, we have generated a partial list of the physiological variables that are homeostatically regulated ( Table 1 ). The list of widely recognized and clearly established regulated variables in humans includes a number of inorganic ions (e.g., H + , Ca 2+ , K + , and Na + ), blood-borne nutrients (e.g., glucose), blood pressure, blood volume, blood osmolarity, and core body temperature.

Table 1.

Homeostatically regulated variables typically found in undergraduate human physiology textbooks

Regulated VariableNormal Range or ValueSensor (Location If Known)Control Center (Location)EffectorsEffector Response
Arterial P o 275� mmHgChemosensors (carotid bodies and aortic body)Brain stemDiaphragm and respiratory musclesChange breathing frequency and tidal volume
Arterial P co 234� mmHgChemosensors (carotid bodies, aortic body, and the medulla)Brain stemDiaphragm and respiratory musclesChange breathing frequency and tidal volume
K + concentration3.5𠄵.0 meq/lChemosensors (adrenal cortex)Adrenal cortexKidneysAlter reabsorption/secretion of K +
Ca 2+ concentration4.3𠄵.3 meq/l (ionized)Chemosensors (parathyroid gland)Parathyroid glandBone, kidney, and intestineAlter reabsorption of Ca 2+ , alter resorption/building of bone, and alter absorption of Ca 2+
H + concentration (pH)35� nM (pH 7.35𠄷.45)Chemosensors (carotid bodies, aortic body, and floor of the fourth ventricle)Brain stemDiaphragm and respiratory musclesChange breathing frequency and tidal volume and change secretion/reabsorption of H + /bicarbonate ions
Chemosensors (kidney)KidneyKidney
Blood glucose concentration70� mg/dlFed state: chemosensors (pancreas)PancreasLiver, adipose tissue, and skeletal muscleAlter storage/metabolism/release of glucose and its related compounds
Fasting state: chemosensors (hypothalamus, pancreas)Hypothalamus
Core body temperature98.6ଏThermosensors (hypothalamus, skin)HypothalamusBlood vessels and sweat glands in the skin as well as skeletal musclesChange peripheral resistance, rate of sweat secretion rate, and shivering
Alter heat gains/losses
Mean arterial pressure93 mmHgMechanosensors (carotid sinus and aortic arch)MedullaHeart and blood vesselsAlter heart rate, peripheral resistance, inotropic state of the heart, and venomotor tone
Blood volume (effective circulating volume)5 litersMechanosensorsMedullaHeartAlter heart rate, peripheral resistance, and inotropic state of the heart
(Blood vessels: carotid bodies)HypothalamusBlood vesselsAlter Na + and water reabsorption
(Heart: atria and ventricle)AtriaKidneysAlter water absorption
(Kidney: juxtaglomerular apparatus and renal afferent arterioles)KidneyIntestine
Blood osmolality280� mosM/kgOsmosensors (hypothalamus)HypothalamusKidneysAlter water reabsorption

This table includes commonly found components of control systems involved in physiological regulation (i.e., homeostasis). This is not meant to be an exhaustive list but rather reflect the current understanding of homeostatically regulated variables that undergraduate physiology students should understand and be able to apply to problems (e.g., making predictions about responses to perturbations or explaining symptoms of disease).

A potential sticky point occurs when textbooks identify variables as homeostatically regulated even though the system involved does not have all of the required components. The proposition that certain metabolic waste products (e.g., nitrogenous wastes, bilirubin, and creatinine) are homeostatically regulated illustrates such a failure. We are not suggesting that the levels of these substances are not kept relatively constant by steady-state processes in the body. Rather, the concentrations of these substances are not maintained by a system that meets the definition of a homeostatic mechanism listed above. The body does not possess a physiological sensor for detecting these substances in the ECF and therefore cannot homeostatically regulate the ECF concentration of these substances.

Conversely, some mechanisms for controlling the level of a physiological variable include one component of the model (e.g., negative feedback) and may give the appearance of homeostatic regulation but, in the final analysis, do not meet all criteria and should not be considered homeostatic. For example, textbook diagrams illustrating control of blood cortisol levels show several negative feedback loops. This can cause students to think that cortisol is a regulated variable. However, the sensed variable(s) in this system is(are) the variables (e.g., blood glucose or “stress”) whose values are processed by the higher brain centers or hypothalamus and result in the release of corticotropin-releasing hormone. The result of the negative feedback loops involving adrenocorticotropic hormone and cortisol is a modulation of the release rate of the respective hormones. Therefore, corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol should not be considered homeostatically regulated variables. They are signaling elements controlling the effectors that determine the value of the regulated variable(s).

Another possible source of confusion about the identification of regulated variables arises when a physiological variable is regulated under one set of circumstances but behaves as a controlled variable under other circumstances. This can happen if a regulated variable is under the control of two different homeostatic systems or if a regulated variable can be 𠇌oopted” by another homeostatic system. This often happens if a physiological variable plays a role in more than one function in the body.

It is here that the concept of nested homeostasis or hierarchies of homeostats can be helpful. Carpenter (7) has pointed out that there are circumstances in which the maintenance of one regulated variable at its set point value is more important for continued viability of the organism than the simultaneous regulation of another variable.

One example of this is provided by the value of P co 2 in the ECF. As a variable in the internal environment that affects cell viability, P co 2 meets all of the criteria for a homeostatically regulated variable. P co 2 in the ECF depends on the action of respiratory muscles that alter the rate and depth of ventilation. As such, P co 2 in the ECF is maintained within defined limits by a regulatory system that senses P co 2 and operates by negative feedback. However, as any student of acid-base physiology knows, P co 2 in the ECF is not maintained relatively constant during compensatory adjustments in the acid-base balance of the body. From the perspective of H + homeostasis, P co 2 functions as a controlled variable.

At this point, some of our students might ask “Which is it? Is P co 2 a regulated variable or is it a controlled variable?” Our answer is that P co 2 is 𠇋oth,” and we can explain this using the idea of nested homeostatic mechanisms. There are circumstance in which it is more important to maintain arterial H + concentration (pH) in the normal range that maintaining a constant P co 2, perhaps because of the particular impact of the H + concentration on cell survival. Therefore, effective regulation of the H + concentration of the ECF can only be achieved by allowing P co 2 to dramatically vary from its normal range during acid-base disturbances. By introducing the concept of nested homeostatic mechanisms, we have refined how we view P co 2 as a homeostatically regulated variable, and we have offered another way to resolve other, “sticky” situations where the authenticity of a homeostatically regulated variable might be called into question.

Best Practices in Teaching Homeostasis

Given the centrality of the concept of homeostasis (15, 16), one would expect that both instructional resources and instructors would provide a consistent model of the concept and apply this model to appropriate systems in which variables are sensed and maintained relatively constant.

However, examination of undergraduate textbooks revealed that this is not the case (17). The problems found include, but were not limited to, inconsistent language used to describe the phenomenon and incomplete or inadequate pictorial representations of the model. In addition, texts often define homeostasis early in the narrative but fail to reinforce application of the model when specific regulatory mechanisms are discussed (17).

Furthermore, our work focusing on developing a concept inventory for homeostatic regulation (12, 13) revealed considerable confusion among faculty members regarding the concept. We think this confusion may stem, in part, from the level of faculty uncertainty about the concept and degree of complexity of homeostatic regulatory mechanisms. Our discussion of the sticky points associated with homeostasis is an attempt to suggest potential sources of this confusion and to indicate ways that instructors can work through these difficulties.

How do we ameliorate this situation? We propose five strategies that will help in approaching the problem.

1. Faculty members members should adopt a standard set of terms associated with the model. There is inconsistency within and among textbooks with respect to the names for critical components of the model. We propose the terminology shown in Table 2 to be used when discussing homeostatic regulatory mechanisms.

Table 2.

Definitions of terms for homeostasis paper

Control center (or integrator)The control center consists of an error detector and controller. It receives signals (information) from sensors, compares information (value of regulated variable) with the set point, integrates information from all sensors, and sends output signals (sends instructions or commands) to increase or decrease the activity of effectors. The control center determines and initiates the appropriate physiological response to any change or disturbance of the internal environment
ControllerThe component of the control center that receives signals (information) from the error detector and sends output signals (instructions or commands) to increase or decrease the activity of effectors. The controller initiates the appropriate physiological response to an error signal resulting from a change or disturbance of the regulated (sensed) variable.
EffectorA component whose activity or action contributes to determining the value of any variable the system. In this model, the effectors determine the value of the regulated (sensed) variable.
Error detectorThe component in the control center that determines (calculates) the difference between the set point value and the actual value of the regulated (sensed) variable. The error detector generates the error signal that is used to determine the output of the control center.
Error signalA signal that represents the difference between the set point value and the actual value of the regulated variable. The error signal is one of the input signals to the controller.
External environmentThe world outside of the body and its “state.” The state or conditions in the outside world can determine the state of many internal properties of the organism.
IntegratorThis is another term for the control center. The integrator processes information from the sensor and those components that determine the set point, determines any error signal present, and sends output signals (instructions or commands) to increase or decrease the activity of effectors.
Internal environmentThe internal environment is the extracellular fluid compartment. This is the environment in which the body's cells live. It is what Bernard meant by the “internal milieu.”
HomeostasisThe maintenance of a relatively stable internal environment by an organism in the face of a changing external environment and varying internal activity using negative feedback mechanisms to minimize an error signal.
Negative feedbackA control mechanism where the action of the effector (response) opposes a change in the regulated variable and returns it back toward the set point value.
Nonregulated variable (controlled variable)A variable whose value changes in response to effector activity but whose value is not directly sensed by the system. Controlled variables contribute to determination of the regulated variable. For example, heart rate and stroke volume (controlled variables) contribute to determining cardiac output (another controlled variable) that contributes to arterial blood pressure (a regulated variable).
Perturbation (disturbance)Any change in the internal or external environment that causes a change to a homeostatically regulated variable. Physiologically induced changes in the set point would not be considered a perturbation.
Regulated variable (sensed variable)Any variable for which sensors are present in the system and the value of which is kept within limits by a negative feedback system in the face of perturbations in the system. A regulated variable is any property or condition of the extracellular fluid that is kept relatively constant in the internal environment in order to ensure the viability (survival) of the organism.
ResponseThe change in the function or action of an effector.
Sensor (Receptor)A �vice” that measures the magnitude of some variable by generating an output signal (neural or hormonal) that is proportional to the magnitude of the stimulus. A sensor is a measuring �vice.” For some regulated variables, sensors are specialized sensory cells or “sensory receptors,” e.g., thermoreceptors, baroreceptors, or osmoreceptors. For other regulated variables, sensors are cellular components, e.g., the Ca 2+ -sensing receptor (a G protein-coupled receptor that senses blood Ca 2+ in the parathyroid gland).
Set pointThe range of values (range of magnitudes) of the regulated variable that the system attempts to maintain. Set point refers to the �sired value.” The set point is generally not a single value it is a range of values.

A glossary of terms used in discussing the core concept of homeostasis. The components of a homeostatically regulated system ( Fig. 1 ) are defined here as are some other terms that occur in teaching this concept.

2. A standard standard pictorial representation of the model should be adopted when initially explaining homeostasis, and it should be used to frame the discussion of the specific system being considered. Figure 1 shows such a diagram.

The argument could be made that this diagram may be difficult for undergraduate students to understand. This may be the rationale for presenting the much-simplified diagrams found in most undergraduate texts (17). However, because these simple diagrams do not explicitly include all components of a homeostatic regulatory system (e.g., a set point), they may be a source of the misconceptions discussed as sticky points. As a result, students may not recognize that an essential feature of homeostatic regulatory systems is minimizing an error signal. A simplified representation of the model that includes the critical components of the regulatory system is shown in Fig. 2 . Depending on the course content and level of the student, this model can be expanded to add more levels of complexity as are required.

Simplified representation of a homeostatic regulatory system. Several components shown in Fig. 1 are combined in this representation. The reader should refer to Table 1 to find correspondence between components of physiologically significant homeostatic regulatory systems and this simplified representation. For example, chemosensors in the carotid bodies and aortic body are “sensors,” the brain stem is the 𠇌ontrol center,” and the diaphragm and other respiratory muscles are �tors” in the homeostatic regulatory system for arterial P o 2.

3. Faculty members should introduce the concept of homeostatic regulation early in the course and continue to apply and hence reinforce the model as each new homeostatic system is encountered. It is important to continue to use the standard terminology and visual representation as recommended in the first and second points above. Students tend to neither spontaneously or readily generalize their use of core concepts. It is therefore incumbent on the instructor to create a learning environment where this kind of transfer behavior is promoted. Faculty members can facilitate this by providing multiple opportunities for students to test and refine their understanding of the core concept of homeostatic regulation.

One way to reinforce the broad application of the model of homeostasis and help students demonstrate that they understand any particular homeostatic mechanism is to have them ask (and answer) a series of questions about each of homeostatically regulated systems they encounter (see Table 3 ). In doing so, they demonstrate that they can determine the essential components of the mental model needed to define the homeostatic system. The effort to thoroughly and accurately answer these questions will help students uncover gaps in their understanding and will reveal uncertainties in the resource information that they are using.

Table 3.

Questions students should ask about any homeostatically regulated system

What is the homeostatically regulated variable? Is it a property or condition of the extracellular fluid?
What and where is the sensor?
What and where is the control center?
What and where is the effector(s)? How do they alter their activities so as to produce a response?
Does the response lead to a change in the regulated variable/stimulus consistent with error signal reduction (negative feedback)?

4. Faculty members should use care when they select and explain the physiological examples or analogical models they chose to introduce and illustrate homeostasis in the classroom. In particular, instructors should ensure that the representative examples they use do not introduce additional misconceptions into student thinking. This is especially so when thermoregulation may be considered as an example of homeostatic regulation.

An informal survey of physiology textbooks indicated that thermoregulation is almost universally used as an example of a homeostatic mechanism. The most likely reasons for this selection are that 1) there is an everyday, seemingly easy to understand process involving the regulation of air temperature in room or building (i.e., the operation of a furnace and an air conditioner) and 2) the body's physiological responses are commonly and obviously observable and/or experienced by the learner (sweating, shivering, and changes in skin coloration). However, based on our description of the typical homeostatic regulatory system, there are compelling reasons to recommend that caution be taken if thermoregulation is used as the initial and representative example of homeostasis.

Most concerning, the typical home heating and cooling system operates in a manner that is distinctly different from mechanisms of human thermoregulation. The effectors in most houses, the furnace and air conditioner, operate in a full-on/full-off manner. For example, when the temperature at the thermostat falls below the value that has been dialed in (the set point temperature), the furnace turns on and stays on at maximum output until the temperature returns to the set point value. However, this is not how the human thermoregulatory system functions or how other homeostatic mechanisms operate. One potential consequence of using this model system to illustrate a homeostatic system is the creation of a common student misconception that homeostatic mechanisms operate in an on/off manner (12, 24), a sticky point we have addressed above. Faculty members need to help students overcome this problem area if they chose to use thermoregulation as a representative example of homeostasis.

What alternatives might be recommended? We suggest the automobile cruise control as a helpful nonbiological analog for homeostasis. The use of cruise control is not an uncommon activity for students, and, as we have described previously, the operation of a cruise control is theoretically easy to understand. What about a physiological example to represent homeostasis? A review of Table 1 would suggest the insulin-mediated system for blood glucose regulation during the fed state has much to recommend it. Students are generally familiar with the particulars of the system from either previous coursework or from personal experience. Other systems are likely to be less accessible to the beginning student of physiology.

However, faculty members should be aware that blood glucose regulation is not without its downsides as a representative example of homeostatic regulation. It is not easy to identify or explain the operation of the glucose sensor, the set point, and the controller involved in glucose homeostasis. Furthermore, there is probably no widely understood analog to glucose regulation that can be easily drawn from everyday life. Neither cruise controls, navigation systems on airplanes, autofocuses on cameras or other common, nor everyday examples of servomechanisms fully correspond to the operation of the feedback system involved in regulating blood glucose during the fed state. This points out the tradeoffs that must be made when any particular example or model is adopted to represent homeostatic regulation. Recognizing this, the use of a physiological control system such as glucose regulation during the fed state, where the effectors operate continuously, seems preferable to thermoregulation as a representative example for teaching the concept of homeostatic regulation.

5. When discussing discussing organismal physiology, restrict the use of the term “homeostatic regulation” to mechanisms related to maintaining consistency of the internal environment (i.e., the ECF).

Adopting these five strategies will provide students with a consistent framework for building their own mental models of specific homeostatic mechanisms and will help them recognize the functional similarities among different homeostatic regulatory systems at the organismal level. Because of its widespread application to different systems in organismal biology, homeostasis is one of the most important unifying ideas in physiology (15, 16). To construct a robust and enduring understanding of this concept, students need the proper tools. By giving them a precise and consistent terminology and encouraging them to use a standardized pictorial representation of the homeostatic model, we enable them to build a proper foundation for comprehending homeostatic systems. By making students aware of the potential sources of confusion surrounding the concept of homeostasis, i.e., the sticky points, we help prevent their thinking from becoming misguided or out of square. By doing so, we set the stage for our students to develop an accurate understanding of a wide range of physiological phenomena and to arrive at an integrated sense of the “wisdom of the body.”

How Does Homeostasis Control Heart Rate?

Homeostasis regulates the heart rate and all of its internal functions to maintain equilibrium. According to Biology Online, homeostasis uses a negative and positive feedback system to keep the human body running efficiently.

The portion of the brain stem that controls the heart rate is the medulla. The medulla transmits chemical messages and nerve impulses through the medulla pyramids. According to, the medulla pyramids are where all communication for the muscles, organs, and other areas of the body take place. During exercise and periods of high activity, the muscles in your body send messages through the brain stem to the medulla. The medulla then releases two hormones, epinephrine and norepinephrine, which travel through the brain stem to the heart. Once those two hormones reach the sinus node, they stimulate electrical impulses in the heart muscles and cause the heart muscle to contract faster.

When you stop exercising or decrease your level of activity, the muscles in the body send another message to the medulla to release acetylcholine.This hormone slows down the contractions of the heart, and allows the heart to rest by reducing the heart rate.

According to Biology Online, each beat of the heart pumps blood and oxygen to the muscles and organs of the body, so they can function properly. While oxygen is being delivered throughout the body, carbon dioxide is being removed to keep all of the cells, organs, muscles, and blood clean and healthy.

Disease as Homeostatic Imbalance

If positive and negative feedback loops are affected or altered, homeostatic imbalance and resultant complications can occur.

Learning Objectives

Analyze disease as a result of homeostatic imbalance

Key Takeaways

Key Points

  • Many diseases are a result of homeostatic imbalance, an inability of the body to restore a functional, stable internal environment.
  • Aging is a source of homeostatic imbalance as the control mechanisms of the feedback loops lose their efficiency, which can cause heart failure.
  • Diseases that result from a homeostatic imbalance include heart failure and diabetes, but many more examples exist.
  • Diabetes occurs when the control mechanism for insulin becomes imbalanced, either because there is a deficiency of insulin or because cells have become resistant to insulin.
  • Homeostasis is the ability of a system to regulate its internal environment through maintaining a stable, relatively constant set of properties such as temperature and pH.

Key Terms

  • homeostasis: The ability of a system or living organism to adjust its internal environment to maintain a stable equilibrium, such as the ability of warm-blooded animals to maintain a constant body temperature.
  • diabetes: A group of metabolic diseases in which a person or animal has high blood sugar due to an inability to produce, metabolize, or respond to insulin.
  • blood sugar regulation: Carbohydrate and fat metabolism are regulated by insulin, a hormone produced by the pancreas.

What Is Disease?

Disease is any failure of normal physiological function that leads to negative symptoms. While disease is often a result of infection or injury, most diseases involve the disruption of normal homeostasis. Anything that prevents positive or negative feedback from working correctly could lead to disease if the mechanisms of disruption become strong enough.

Aging is a general example of disease as a result of homeostatic imbalance. As an organism ages, weakening of feedback loops gradually results in an unstable internal environment. This lack of homeostasis increases the risk for illness and is responsible for the physical changes associated with aging. Heart failure is the result of negative feedback mechanisms that become overwhelmed, allowing destructive positive feedback mechanisms to compensate for the failed feedback mechanisms. This leads to high blood pressure and enlargement of the heart, which eventually becomes too stiff to pump blood effectively, resulting in heart failure. Severe heart failure can be fatal.

Diabetes: A Disease of Failed Homeostasis

Diabetes, a metabolic disorder caused by excess blood glucose levels, is a key example of disease caused by failed homeostasis. In ideal circumstances, homeostatic control mechanisms should prevent this imbalance from occurring. However, in some people, the mechanisms do not work efficiently enough or the amount of blood glucose is too great to be effectively managed. In these cases, medical intervention is necessary to restore homeostasis and prevent permanent organ damage.

Blood Sugar Regulation

The human body maintains constant levels of glucose throughout the day, even after fasting. During long periods of fasting, glucose levels are reduced only very slightly. Insulin transports glucose to the body’s cells for use in cellular metabolic function. The cells convert excess glucose to an insoluble substance called glycogen to prevent it from interfering with cellular metabolism. Because this ultimately lowers blood glucose levels, insulin is secreted to prevent hyperglycemia (high blood sugar levels). Another hormone called glucagon performs the opposite function of insulin, causing cells to convert glycogen to glucose and stimulating new glucose production (gluconeogenesis) to raise blood sugar levels. Negative feedback between insulin and glucagon levels controls blood sugar homeostasis.

Causes of Homeostatic Disruption

People with type 1 diabetes do not produce insulin due to auto-immune destruction of the insulin producing cells, while people with type 2 diabetes have chronic high blood glucose levels that cause insulin resistance. With diabetes, blood glucose is increased by normal glucagon activity, but the lack of or resistance to insulin means that blood sugar levels are unable to return to normal. This causes metabolic changes that result in diabetes symptoms like weakened blood vessels and frequent urination. Diabetes is normally treated with insulin injections, which replaces the missing negative feedback of normal insulin secretions.

Homeostasis of Glucose Metabolism: This image illustrates glucose metabolism over the course of a day. Homeostasis may become imbalanced if the pancreas is overly stressed, making it unable to balance glucose metabolism. This can lead to diabetes.


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Homeostasis, any self-regulating process by which biological systems tend to maintain stability while adjusting to conditions that are optimal for survival. If homeostasis is successful, life continues if unsuccessful, disaster or death ensues. The stability attained is actually a dynamic equilibrium, in which continuous change occurs yet relatively uniform conditions prevail.

What is homeostasis?

Homeostasis is any self-regulating process by which an organism tends to maintain stability while adjusting to conditions that are best for its survival. If homeostasis is successful, life continues if it’s unsuccessful, it results in a disaster or death of the organism. The “stability” that the organism reaches is rarely around an exact point (such as the idealized human body temperature of 37 °C [98.6 °F]). Stability takes place as part of a dynamic equilibrium, which can be thought of as a cloud of values within a tight range in which continuous change occurs. The result is that relatively uniform conditions prevail.

What is an example of homeostasis in a living thing?

Body temperature control in humans is one of the most familiar examples of homeostasis. Normal body temperature hovers around 37 °C (98.6 °F), but a number of factors can affect this value, including exposure to the elements, hormones, metabolic rate, and disease, leading to excessively high or low body temperatures. The hypothalamus in the brain regulates body temperature, and feedback about body temperature from the body is carried through the bloodstream to the brain, which results in adjustments in breathing rate, blood sugar levels, and metabolic rate. In contrast, reduced activity, perspiration, and heat-exchange processes that permit more blood to circulate near the skin surface contribute to heat loss. Heat loss is reduced by insulation, decreased circulation to the skin, clothing, shelter, and external heat sources.

What is an example of homeostasis in a mechanical system?

A familiar example of homeostatic regulation in a mechanical system is the action of a thermostat, a machine that regulates room temperature. At the centre of a thermostat is a bimetallic strip that responds to temperature changes. The strip expands under warmer conditions and contracts under cooler conditions to either disrupt or complete an electric circuit. When the room cools, the circuit is completed, the furnace switches on, and the temperature rises. At a preset level, perhaps 20 °C (68 °F), the circuit breaks, the furnace stops, and no additional heat is released into the room. Over time, the temperature slowly drops until the room cools enough to trigger the process again.

Are there examples of homeostasis in ecosystems?

The concept of homeostasis has also been used in studies of ecosystems. Canadian-born American ecologist Robert MacArthur first proposed in 1955 that homeostasis in ecosystems results from biodiversity (the variety of life in a given place) and the ecological interactions (predation, competition, decomposition, etc.) that occur between the species living there. The term homeostasis has been used by many ecologists to describe the back-and-forth interaction that occurs between the different parts of an ecosystem to maintain the status quo. It was thought that this kind of homeostasis could help to explain why forests, grasslands, or other ecosystems persist (that is, remain in the same location for long periods of time). Since 1955 the concept has changed to incorporate the ecosystem’s nonliving parts, such as rocks, soil, and water.

Any system in dynamic equilibrium tends to reach a steady state, a balance that resists outside forces of change. When such a system is disturbed, built-in regulatory devices respond to the departures to establish a new balance such a process is one of feedback control. All processes of integration and coordination of function, whether mediated by electrical circuits or by nervous and hormonal systems, are examples of homeostatic regulation.

A familiar example of homeostatic regulation in a mechanical system is the action of a room-temperature regulator, or thermostat. The heart of the thermostat is a bimetallic strip that responds to temperature changes by completing or disrupting an electric circuit. When the room cools, the circuit is completed, the furnace operates, and the temperature rises. At a preset level the circuit breaks, the furnace stops, and the temperature drops. Biological systems, of greater complexity, however, have regulators only very roughly comparable to such mechanical devices. The two types of systems are alike, however, in their goals—to sustain activity within prescribed ranges, whether to control the thickness of rolled steel or the pressure within the circulatory system.

The control of body temperature in humans is a good example of homeostasis in a biological system. In humans, normal body temperature fluctuates around the value of 37 °C (98.6 °F), but various factors can affect this value, including exposure, hormones, metabolic rate, and disease, leading to excessively high or low temperatures. The body’s temperature regulation is controlled by a region in the brain called the hypothalamus. Feedback about body temperature is carried through the bloodstream to the brain and results in compensatory adjustments in the breathing rate, the level of blood sugar, and the metabolic rate. Heat loss in humans is aided by reduction of activity, by perspiration, and by heat-exchange mechanisms that permit larger amounts of blood to circulate near the skin surface. Heat loss is reduced by insulation, decreased circulation to the skin, and cultural modification such as the use of clothing, shelter, and external heat sources. The range between high and low body temperature levels constitutes the homeostatic plateau—the “normal” range that sustains life. As either of the two extremes is approached, corrective action (through negative feedback) returns the system to the normal range.

The concept of homeostasis has also been applied to ecological settings. First proposed by Canadian-born American ecologist Robert MacArthur in 1955, homeostasis in ecosystems is a product of the combination of biodiversity and large numbers of ecological interactions that occur between species. It was thought of as a concept that could help to explain an ecosystem’s stability—that is, its persistence as a particular ecosystem type over time (see ecological resilience). Since then, the concept has changed slightly to incorporate the ecosystem’s abiotic (nonliving) parts the term has been used by many ecologists to describe the reciprocation that occurs between an ecosystem’s living and nonliving parts to maintain the status quo. The Gaia hypothesis—the model of Earth posited by English scientist James Lovelock that considers its various living and nonliving parts as components of a larger system or single organism—makes the assumption that the collective effort of individual organisms contributes to homeostasis at the planetary level. The single-organism aspect of the Gaia hypothesis is considered controversial because it posits that living things, at some level, are driven to work on behalf of the biosphere rather than toward the goal of their own survival.

The Editors of Encyclopaedia Britannica This article was most recently revised and updated by John P. Rafferty, Editor.

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