2. Desórdenes Alimentarios: Anorexia y Bulimia Carlos Hernandez-Cassis, M.D., MPH. Professor of Medicine University of Nevada School of Medicine, Las Vegas VA Southern Nevada Healthcare System
Role of Incretins in Glucose Homeostasis Speaker notes After food is ingested, GIP is released from K cells in the proximal gut (duodenum), and GLP-1 is released from L cells in the distal gut (ileum and colon). 1 – 3 Under normal circumstances, DPP-4 (dipeptidyl-peptidase 4) rapidly degrades these incretins to their inactive forms after their release into the circulation. 1,2 Actions of GLP-1 and GIP include stimulating insulin response in pancreatic beta cells (GLP-1 and GIP) and suppressing glucagon production (GLP-1) in pancreatic alpha cells when the glucose level is elevated. 2,3 The subsequent increase in glucose uptake in muscles 3,4 and reduced glucose output from the liver 2 help maintain glucose homeostasis. Thus, the incretins GLP-1 and GIP are important glucoregulatory hormones that positively affect glucose homeostasis by physiologically helping to regulate insulin in a glucose-dependent manner. 2,3 GLP-1 also helps to regulate glucagon secretion in a glucose-dependent manner. 2,5 References 1. Kieffer TJ, Habener JF. The glucagon-like peptides. Endocr Rev . 1999;20:876–913. 2. Ahrén B. Gut peptides and type 2 diabetes mellitus treatment. Curr Diab Rep . 2003;3:365–372. 3. Drucker DJ. Enhancing incretin action for the treatment of type 2 diabetes. Diabetes Care . 2003;26:2929–2940. 4. Holst JJ. Therapy of type 2 diabetes mellitus based on the actions of glucagon-like peptide-1. Diabetes Metab Res Rev . 2002;18:430–441. 5. Nauck MA, Kleine N, Ørskov C, Holst JJ, Wilms B, Creutzfeldt W. Normalization of fasting hyperglycaemia by exogenous glucagon-like peptide 1 (7-36 amide) in type 2 (non-insulin-dependent) diabetic patients. Diabetologia . 1993;36:741–744. Purpose: To demonstrate how the incretin pathway is part of the normal physiology of glucose homeostasis. Takeaway: After food ingestion, incretins stimulate insulin release from beta cells and suppress glucagon release from alpha cells in a glucose-dependent manner, resulting in downstream effects that regulate glucose homeostasis.