Editing Insulin resistance (section)

===Hormones===
Many hormones can induce insulin resistance including [[cortisol]],<ref>{{cite journal | vauthors = Joseph JJ, Golden SH | title = Cortisol dysregulation: the bidirectional link between stress, depression, and type 2 diabetes mellitus | journal = Annals of the New York Academy of Sciences | volume = 1391 | issue = 1 | pages = 20–34 | date = March 2017 | pmid = 27750377 | pmc = 5334212 | doi = 10.1111/nyas.13217 | bibcode = 2017NYASA1391...20J }}</ref> [[growth hormone]], and [[human placental lactogen]].<ref>{{cite journal | vauthors = Newbern D, Freemark M | title = Placental hormones and the control of maternal metabolism and fetal growth | journal = Current Opinion in Endocrinology, Diabetes and Obesity | volume = 18 | issue = 6 | pages = 409–16 | date = December 2011 | pmid = 21986512 | doi = 10.1097/MED.0b013e32834c800d | s2cid = 24095227 }}</ref>

Cortisol counteracts [[insulin]] and can lead to increased hepatic [[gluconeogenesis]], reduced peripheral utilization of glucose, and increased insulin resistance.<ref name="brown">{{Cite book| vauthors = Brown DD|title=USMLE Step 1 Secrets|year=2003 |page=63}}</ref> It does this by decreasing the translocation of [[glucose transporter]]s (especially [[GLUT4]]) to the cell membrane.<ref>{{Cite book|vauthors = King MW|title= Lange Q&A USMLE Step 1|edition= 6th|page= [https://archive.org/details/langeqausmlestep0005unse/page/82 82]|isbn= 978-0-07-144578-8|year= 2005|publisher= McGraw-Hill Medical|location= New York|url-access= registration|url= https://archive.org/details/langeqausmlestep0005unse/page/82}}</ref><ref>{{cite journal | vauthors = Piroli GG, Grillo CA, Reznikov LR, Adams S, McEwen BS, Charron MJ, Reagan LP | title = Corticosterone impairs insulin-stimulated translocation of GLUT4 in the rat hippocampus | journal = Neuroendocrinology | volume = 85 | issue = 2 | pages = 71–80 | year = 2007 | pmid = 17426391 | doi = 10.1159/000101694 | s2cid = 38081413 }}</ref>

Based on the significant improvement in insulin sensitivity in humans after [[bariatric surgery]] and rats with surgical removal of the [[duodenum]],<ref>{{cite journal | vauthors = Garrido-Sanchez L, Murri M, Rivas-Becerra J, Ocaña-Wilhelmi L, Cohen RV, Garcia-Fuentes E, Tinahones FJ | title = Bypass of the duodenum improves insulin resistance much more rapidly than sleeve gastrectomy | journal = Surgery for Obesity and Related Diseases | volume = 8 | issue = 2 | pages = 145–50 | year = 2012 | pmid = 21570362 | doi = 10.1016/j.soard.2011.03.010 }}</ref><ref>{{cite news|url=http://www.mdedge.com/familypracticenews/article/109286/gastroenterology/duodenal-resurfacing-achieves-metabolic-benefits|title=Duodenal resurfacing achieves metabolic benefits in type 2 diabetes|vauthors =Goodman A|date=June 1, 2016|access-date=12 March 2017|agency=Family Practice News}}</ref> it has been proposed that some substance is produced in the [[mucosa]] of that initial portion of the small intestine that signals body cells to become insulin resistant. If the producing tissue is removed, the signal ceases and body cells revert to normal insulin sensitivity. No such substance has been found as yet, and the existence of such a substance remains speculative.{{Citation needed|date=October 2010}}

[[Leptin]] is a hormone produced from the ob gene and adipocytes.<ref name="pmid10766249">{{cite journal | vauthors = Friedman JM | title = Obesity in the new millennium | journal = Nature | volume = 404 | issue = 6778 | pages = 632–4 | date = April 2000 | pmid = 10766249 | doi = 10.1038/35007504 | s2cid = 4406498 | doi-access = free }}</ref> Its physiological role is to regulate hunger by alerting the body when it is full.<ref name=":2">{{cite journal | vauthors = Flier JS | title = Clinical review 94: What's in a name? In search of leptin's physiologic role | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 83 | issue = 5 | pages = 1407–13 | date = May 1998 | pmid = 9589630 | doi = 10.1210/jcem.83.5.4779 | doi-access = free }}</ref> Studies show that lack of leptin causes severe obesity and is strongly linked with insulin resistance.<ref>{{cite journal | vauthors = Elmquist JK, Maratos-Flier E, Saper CB, Flier JS | title = Unraveling the central nervous system pathways underlying responses to leptin | journal = Nature Neuroscience | volume = 1 | issue = 6 | pages = 445–50 | date = October 1998 | pmid = 10196541 | doi = 10.1038/2164 | s2cid = 7474447 }}</ref>