{"id":1615204,"date":"2022-04-02T00:13:36","date_gmt":"2022-04-02T04:13:36","guid":{"rendered":"https:\/\/myendoconsult.com\/learn\/?p=1615204"},"modified":"2023-03-16T05:38:18","modified_gmt":"2023-03-16T10:38:18","slug":"what-is-the-incretin-effect","status":"publish","type":"post","link":"https:\/\/myendoconsult.com\/learn\/what-is-the-incretin-effect\/","title":{"rendered":"What is the Incretin Effect"},"content":{"rendered":"<p><strong>Incretins are gut-derived factors that enhance insulin release<\/strong> by pancreatic beta cells. These factors are produced by <em>selective posttranslational modification of proglucagon<\/em>, a 160-residue peptide expressed by the <strong>\u03b1-cells of the pancreas, K<\/strong> and <strong>L cells of the small intestine<\/strong>.<\/p>\n<p>The incretin effect is described as enhanced insulin secretion in response to an oral glucose load (\u223c6\u20131.7-fold) compared with intravenous glucose administration. <strong>The incretin effect <\/strong>is mainly attributed to the action of two hormones gut hormones, including <em>glucose-dependent insulinotropic peptide (GIP)<\/em> and <em>glucagon-like peptide 1 (GLP-1). <\/em>K cells are responsible for the production of GIP and the L cells for GLP-1.<\/p>\n<h2>What do incretins do?<\/h2>\n\n<table id=\"tablepress-43\" class=\"tablepress tablepress-id-43\">\n<tbody>\n<tr class=\"row-1\">\n\t<td class=\"column-1\">GLP-1<\/td><td class=\"column-2\">\u2022\tGLP-1 is released in the gut in proportion to ingested calories.<br \/>\n\u2022\tReduction in gastric emptying and suppression of gastric acid secretion<br \/>\n\u2022\tAnorexegenic effects<\/td>\n<\/tr>\n<tr class=\"row-2\">\n\t<td class=\"column-1\">Glucose-dependent insulinotropic polypeptide (GIP)<\/td><td class=\"column-2\">\u2022\tAlong with GLP-1, GIP acts as an incretin to potentiate glucose-stimulated insulin release<br \/>\n\u2022\tdirect anabolic effects on adipose tissue, including<br \/>\no\tstimulation of glucose import<br \/>\no\tfatty acid synthesis<br \/>\no\tLipogenesis<br \/>\no\tinhibition of lipolysis<br \/>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<!-- #tablepress-43 from cache -->\n<h2>What are incretin mimetics?<\/h2>\n<p><em>Incretin mimetics mimic the effect of the gut hormone GLP-1 or GIP or both, with favorable metabolic effects in type 2 <a href=\"https:\/\/myendoconsult.com\/learn\/diabetes-mellitus\/\">diabetes mellitus<\/a>. These agents promotes a myriad of effects\u2026<\/em><\/p>\n<ul>\n<li>Suppresses appetite<\/li>\n<li>Inhibits glucose production in the liver<\/li>\n<li>Slows gastric emptying<\/li>\n<li>Stimulates insulin release<\/li>\n<\/ul>\n<ul>\n<li><strong>Glucagon-like peptide 1<\/strong> is an incretin produced from the PROGLUCAGON gene in L cells of the small intestine and is secreted in response to exposure to gastrointestinal nutrients. It is worth noting that GLP-1 is usually deficient in patients with <a href=\"https:\/\/myendoconsult.com\/learn\/egregious-eleven-of-type-2-diabetes-mellitus\/\">type 2 diabetes mellitus<\/a>.<\/li>\n<li>Dipeptidyl peptidase 4 (DPP-4) inhibitors inhibit DPP-4, which is a ubiquitous enzyme expressed on the surface of most cell types that deactivates GLP-1; therefore, its inhibition could potentially affect glucose regulation through multiple effects. DPP4 inhibitors have a very minimal effect on endogenous incretins (GLP-1, GIP)<\/li>\n<li><strong>Dual GLP-1\/GIP agonists<\/strong> (Tirzepatide) \u00a0possess the properties of both incretins and are associated with more significant weight loss than GLP-1 agonist monotherapy.<\/li>\n<\/ul>\n<h2>Mechanism of action of incretins<\/h2>\n<p><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/Mechanism-of-action-incretin-mimetics.png\" sizes=\"auto, (max-width: 1575px) 100vw, 1575px\" srcset=\"https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/Mechanism-of-action-incretin-mimetics.png 1575w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/Mechanism-of-action-incretin-mimetics-300x229.png 300w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/Mechanism-of-action-incretin-mimetics-768x585.png 768w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/Mechanism-of-action-incretin-mimetics-1536x1170.png 1536w, https:\/\/myendoconsult.com\/learn\/wp-content\/uploads\/Mechanism-of-action-incretin-mimetics-624x475.png 624w\" alt=\"\" width=\"1575\" height=\"1200\" \/><\/p>\n<h2>Comparison of incretin drugs<\/h2>\n\n<table id=\"tablepress-44\" class=\"tablepress tablepress-id-44\">\n<tbody>\n<tr class=\"row-1\">\n\t<td class=\"column-1\">DPP-4 inhibitors<\/td><td class=\"column-2\">GLP-1 agonist therapy<\/td>\n<\/tr>\n<tr class=\"row-2\">\n\t<td class=\"column-1\">\u2022\tIncreases endogenous GLP-1 <br \/>\n\u2022\tStimulate glucose-dependent insulin secretion from B cells<br \/>\n\u2022\tLower glucagon secretion<br \/>\n\u2022\tOverall effect -- lowers hepatic glucose output<\/td><td class=\"column-2\">Exert all the effects of DPP-4 agents<br \/>\n\u2022\tSlow gastric emptying<br \/>\n\u2022\tDecrease food intake<br \/>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<!-- #tablepress-44 from cache -->\n<h2>Selected References<\/h2>\n<ul>\n<li>Nauck MA, Meier JJ. Incretin hormones: Their role in health and disease. <a href=\"https:\/\/doi.org\/10.1111\/dom.13129\" target=\"_blank\" rel=\"noopener\">Diabetes Obes Metab. 2018 Feb;20 Suppl 1:5-21.<\/a><\/li>\n<li>Drucker DJ. The biology of incretin hormones.<a href=\"https:\/\/doi.org\/10.1016\/j.cmet.2006.01.004\" target=\"_blank\" rel=\"noopener\"> Cell Metab. 2006 Mar;3(3):153-65.\u00a0<\/a><\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"<p>Incretins are gut-derived factors that enhance insulin release by pancreatic beta cells. These factors are produced by selective posttranslational modification of proglucagon, a 160-residue peptide expressed by the \u03b1-cells of the pancreas, K and L cells of the small intestine. The incretin effect is described as enhanced insulin secretion in response to an oral glucose [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[63,224,50],"tags":[],"class_list":["post-1615204","post","type-post","status-publish","format-standard","hentry","category-endocrineblog","category-diabetes-patients","category-endocrine-disease-diabetes","post-wrapper","thrv_wrapper"],"_links":{"self":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/1615204","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/comments?post=1615204"}],"version-history":[{"count":85,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/1615204\/revisions"}],"predecessor-version":[{"id":4415846,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/posts\/1615204\/revisions\/4415846"}],"wp:attachment":[{"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/media?parent=1615204"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/categories?post=1615204"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/myendoconsult.com\/learn\/wp-json\/wp\/v2\/tags?post=1615204"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}