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All homeostatic control mechanisms have at least three interdependent components for the variable being regulated: a receptor, a control center, and an effector. [3] The receptor is the sensing component that monitors and responds to changes in the environment, either external or internal. Receptors include thermoreceptors and mechanoreceptors.
By inhibiting glucagon release, GLP-1 receptor activation helps to maintain glucose homeostasis. Another important function of the GLP-1 receptor is the regulation of gastric emptying. Activation of the receptor delays the rate at which the stomach empties, leading to increased satiety and reduced food intake.
Receptors may bind with some molecules (ligands) or may interact with physical agents like light, mechanical temperature, pressure, etc. Reception occurs when the target cell (any cell with a receptor protein specific to the signal molecule) detects a signal, usually in the form of a small, water-soluble molecule, via binding to a receptor ...
A taste receptor or tastant is a type of cellular receptor that facilitates the sensation of taste. When food or other substances enter the mouth, molecules interact with saliva and are bound to taste receptors in the oral cavity and other locations. Molecules which give a sensation of taste are considered "sapid". [1]
For example, the emissions of a predator's food source, such as odors or pheromones, may be in the air or on a surface where the food source has been. Cells in the head, usually the air passages or mouth, have chemical receptors on their surface that change when in contact with the emissions.
Energy intake is measured by the amount of calories consumed from food and fluids. [1] Energy intake is modulated by hunger, which is primarily regulated by the hypothalamus, [1] and choice, which is determined by the sets of brain structures that are responsible for stimulus control (i.e., operant conditioning and classical conditioning) and cognitive control of eating behavior.
Low-T3 syndrome and high-T3 syndrome: Consequences of step-up hypodeiodination, e.g. in critical illness as an example for type 1 allostasis, [20] or hyperdeiodination, as in type 2 allostasis, including posttraumatic stress disorder. [12] Resistance to thyroid hormone: Feedback loop interrupted on the level of pituitary thyroid hormone receptors.
A typical example is CXCL-8, which acts as a chemoattractant for neutrophils. In contrast to the homeostatic chemokine receptors, there is significant promiscuity (redundancy) associated with binding receptor and inflammatory chemokines. This often complicates research on receptor-specific therapeutics in this area. [8]