Homeostasis

In biology, homeostasis (British also homoeostasis) (/hɒmɪə(ʊ)ˈsteɪsɪs/) is the state of steady internal, physical, chemical, and social conditions maintained by living systems.[1] This is the condition of optimal functioning for the organism and includes many variables, such as body temperature and fluid balance, being kept within certain pre-set limits (homeostatic range). Other variables include the pH of extracellular fluid, the concentrations of sodium, potassium, and calcium ions, as well as the blood sugar level, and these need to be regulated despite changes in the environment, diet, or level of activity. Each of these variables is controlled by one or more regulators or homeostatic mechanisms, which together maintain life.

Homeostasis is brought about by a natural resistance to change when already in optimal conditions,[2] and equilibrium is maintained by many regulatory mechanisms; it is thought to be the central motivation for all organic action. 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. Control centers include the respiratory center and the renin-angiotensin system. An effector is the target acted on, to bring about the change back to the normal state. At the cellular level, effectors include nuclear receptors that bring about changes in gene expression through up-regulation or down-regulation and act in negative feedback mechanisms. An example of this is in the control of bile acids in the liver.[4]

Some centers, such as the renin–angiotensin system, control more than one variable. When the receptor senses a stimulus, it reacts by sending action potentials to a control center. The control center sets the maintenance range—the acceptable upper and lower limits—for the particular variable, such as temperature. The control center responds to the signal by determining an appropriate response and sending signals to an effector, which can be one or more muscles, an organ, or a gland. When the signal is received and acted on, negative feedback is provided to the receptor that stops the need for further signaling.[5]

The cannabinoid receptor type 1 (CB1), located at the presynaptic neuron, is a receptor that can stop stressful neurotransmitter release to the postsynaptic neuron; it is activated by endocannabinoids (ECs) such as anandamide (N-arachidonoylethanolamide; AEA) and 2-arachidonoylglycerol (2-AG) via a retrograde signaling process in which these compounds are synthesized by and released from postsynaptic neurons, and travel back to the presynaptic terminal to bind to the CB1 receptor for modulation of neurotransmitter release to obtain homeostasis.[6]

The polyunsaturated fatty acids (PUFAs) are lipid derivatives of omega-3 (docosahexaenoic acid, DHA, and eicosapentaenoic acid, EPA) or of omega-6 (arachidonic acid, ARA) are synthesized from membrane phospholipids and used as a precursor for endocannabinoids (ECs) mediate significant effects in the fine-tuning adjustment of body homeostasis.[7]

  1. ^ Gordon Betts, J. Anatomy and physiology. DeSaix, Peter., Johnson, Eddie., Johnson, Jody E., Korol, Oksana., Kruse, Dean H., Poe, Brandon. Houston, Texas. p. 9. ISBN 978-1-947172-04-3. OCLC 1001472383.{{cite book}}: CS1 maint: multiple names: authors list (link)
  2. ^ Martin E (2008). A dictionary of biology (6th ed.). Oxford: Oxford University Press. pp. 315–316. ISBN 978-0-19-920462-5.
  3. ^ Biology Online (27 October 2019). "Homeostasis". Biology Online. Archived from the original on 12 August 2020. Retrieved 27 October 2019.
  4. ^ Kalaany NY, Mangelsdorf DJ (2006). "LXRS and FXR: the yin and yang of cholesterol and fat metabolism". Annual Review of Physiology. 68: 159–91. doi:10.1146/annurev.physiol.68.033104.152158. PMID 16460270.
  5. ^ Cite error: The named reference Marieb was invoked but never defined (see the help page).
  6. ^ Lovinger DM (2008), "Presynaptic Modulation by Endocannabinoids", in Südhof TC, Starke K (eds.), Pharmacology of Neurotransmitter Release, Handbook of Experimental Pharmacology, vol. 184, Springer Berlin Heidelberg, pp. 435–477, doi:10.1007/978-3-540-74805-2_14, ISBN 978-3-540-74805-2, PMID 18064422
  7. ^ Freitas HR, Isaac AR, Malcher-Lopes R, Diaz BL, Trevenzoli IH, Reis RA (26 November 2018). "Polyunsaturated fatty acids and endocannabinoids in health and disease". Nutritional Neuroscience. 21 (10): 695–714. doi:10.1080/1028415X.2017.1347373. ISSN 1028-415X. PMID 28686542. S2CID 40659630.

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