Jump to content
Main menu
Main menu
move to sidebar
hide
Navigation
Main page
Recent changes
Random page
Help about MediaWiki
Special pages
Niidae Wiki
Search
Search
Appearance
Create account
Log in
Personal tools
Create account
Log in
Pages for logged out editors
learn more
Contributions
Talk
Editing
Homeostasis
(section)
Page
Discussion
English
Read
Edit
View history
Tools
Tools
move to sidebar
hide
Actions
Read
Edit
View history
General
What links here
Related changes
Page information
Appearance
move to sidebar
hide
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
===Blood glucose=== {{Main |Blood sugar regulation |Glycolysis#Regulation of the rate limiting enzymes}} [[File:Negative Feedback Gif.gif|thumb|300px|[[Negative feedback]] at work in the regulation of blood sugar. Flat line is the set-point of glucose level and sine wave the fluctuations of glucose.]] [[Blood sugar]] levels are [[Blood sugar regulation|regulated]] within fairly narrow limits.<ref>{{Cite book|last=Bhagavan|first=N. V.|title=Medical biochemistry|edition=4th|publisher=[[Academic Press]]|year=2002|page=499|url=https://books.google.com/books?id=vT9YttFTPi0C&pg=PA499|isbn=978-0-12-095440-7|access-date=21 October 2020|archive-date=6 March 2022|archive-url=https://web.archive.org/web/20220306112840/https://books.google.com/books?id=vT9YttFTPi0C&pg=PA499|url-status=live}}</ref> In mammals, the primary sensors for this are the [[beta cells]] of the [[pancreatic islets]].<ref name=koeslag>{{cite journal |last1=Koeslag |first1=Johan H. |last2=Saunders |first2=Peter T. |last3=Terblanche |first3=Elmarie | title=Topical Review: A reappraisal of the blood glucose homeostat which comprehensively explains the type 2 diabetes-syndrome X complex |journal=Journal of Physiology | publication-date=2003 |volume= 549|issue=Pt 2 |pages=333β346 |doi=10.1113/jphysiol.2002.037895 |pmid=12717005 |pmc=2342944 |year=2003}}</ref><ref name=stryer>{{cite book |last1= Stryer |first1= Lubert | title=Biochemistry. |edition= Fourth |location= New York |publisher= W.H. Freeman and Company|date= 1995 |pages=164, 773β774|isbn= 0-7167-2009-4 }}</ref> The beta cells respond to a rise in the blood sugar level by secreting [[insulin]] into the blood and simultaneously inhibiting their neighboring [[alpha cells]] from secreting [[glucagon]] into the blood.<ref name=koeslag /> This combination (high blood insulin levels and low glucagon levels) act on effector tissues, the chief of which is the [[liver]], [[fat cells]], and [[muscle cells]]. The liver is inhibited from producing [[glucose]], taking it up instead, and converting it to [[glycogen]] and [[triglycerides]]. The glycogen is stored in the liver, but the triglycerides are secreted into the blood as [[very low-density lipoprotein]] (VLDL) particles which are taken up by [[adipose tissue]], there to be stored as fats. The fat cells take up glucose through special glucose transporters ([[GLUT4]]), whose numbers in the cell wall are increased as a direct effect of insulin acting on these cells. The glucose that enters the fat cells in this manner is converted into triglycerides (via the same metabolic pathways as are used by the liver) and then stored in those fat cells together with the VLDL-derived triglycerides that were made in the liver. Muscle cells also take glucose up through insulin-sensitive GLUT4 glucose channels, and convert it into muscle glycogen.<ref>{{Cite journal |last1=Richter |first1=Erik A. |last2=Hargreaves |first2=Mark |date=July 2013 |title=Exercise, GLUT4, and Skeletal Muscle Glucose Uptake |url=https://www.physiology.org/doi/10.1152/physrev.00038.2012 |journal=Physiological Reviews |language=en |volume=93 |issue=3 |pages=993β1017 |doi=10.1152/physrev.00038.2012 |pmid=23899560 |issn=0031-9333}}</ref> A fall in blood glucose, causes insulin secretion to be stopped, and [[glucagon]] to be secreted from the alpha cells into the blood. This inhibits the uptake of glucose from the blood by the liver, fats cells, and muscle. Instead the liver is strongly stimulated to manufacture glucose from glycogen (through [[glycogenolysis]]) and from non-carbohydrate sources (such as [[Lactic acid|lactate]] and de-aminated [[amino acids]]) using a process known as [[gluconeogenesis]].<ref>{{Cite journal|last1=Aronoff|first1=Stephen L.|last2=Berkowitz|first2=Kathy|last3=Shreiner|first3=Barb|last4=Want|first4=Laura|date=1 July 2004|title=Glucose Metabolism and Regulation: Beyond Insulin and Glucagon|url=https://spectrum.diabetesjournals.org/content/17/3/183|journal=Diabetes Spectrum|language=en|volume=17|issue=3|pages=183β190|doi=10.2337/diaspect.17.3.183|issn=1040-9165|doi-access=|access-date=19 July 2018|archive-date=3 January 2020|archive-url=https://web.archive.org/web/20200103090044/https://spectrum.diabetesjournals.org/content/17/3/183|url-status=live}}</ref> The glucose thus produced is discharged into the blood correcting the detected error ([[hypoglycemia]]). The glycogen stored in muscles remains in the muscles, and is only broken down, during exercise, to [[glucose-6-phosphate]] and thence to [[pyruvic acid|pyruvate]] to be fed into the [[citric acid cycle]] or turned into [[lactic acid|lactate]]. It is only the lactate and the waste products of the citric acid cycle that are returned to the blood. The liver can take up only the lactate, and, by the process of energy-consuming [[gluconeogenesis]], convert it back to glucose.{{citation needed|date=January 2024}}
Summary:
Please note that all contributions to Niidae Wiki may be edited, altered, or removed by other contributors. If you do not want your writing to be edited mercilessly, then do not submit it here.
You are also promising us that you wrote this yourself, or copied it from a public domain or similar free resource (see
Encyclopedia:Copyrights
for details).
Do not submit copyrighted work without permission!
Cancel
Editing help
(opens in new window)
Search
Search
Editing
Homeostasis
(section)
Add topic