THE ROLE OF HORMONES IN OBESITY
Obesity is a chronic disease characterized by disrupted energy balance, partly driven by altered peripheral hormonal signaling that influences eating behavior2,3
Some of the peripheral hormones regulating eating behavior include ghrelin, which drives hunger, and GLP-1, leptin, insulin, and amylin, which promote satiety and satiation.1
GLP-1
GLP-1 is a nutrient-stimulated intestinal hormone with multiple roles, including appetite regulation.4-6
Ghrelin
Ghrelin is a stomach-derived hormone that stimulates hunger and promotes meal initiation.4
Leptin
Leptin is an adipose-derived hormone that signals long-term energy sufficiency and normally suppresses appetite.4,5
Insulin
Insulin is released from the pancreas in response to meals and helps regulate appetite in the brain.1,4
Amylin
Amylin has a specific role. Amylin is a nutrient-stimulated hormone that plays a role in satiation, glucose regulation, and bone remodeling.7,8
Beyond its role in eating behavior and energy balance, the mechanistic effects of amylin described in preclinical studies include:
Reduction of appetite and energy intake, with increased satiety9
Delayed gastric emptying, and decreased postprandial glucagon secretion7,9,10
Inhibition of osteoclast-mediated bone resorption, thereby supporting bone formation8
Your questions answered about obesity, hormones, and appetite regulation
Ghrelin, amylin, leptin, insulin, and GLP-1 all play a role in appetite regulation.1
Appetite regulation is complex and mediated by activation of multiple receptors. By targeting different receptors, different hormones can have complementary action.1
No. Ghrelin stimulates hunger and promotes meal initiation, while GLP-1 promotes satiety by reducing appetite and slowing gastric emptying. Leptin signals long-term energy stores and normally suppresses appetite, insulin signals energy stores and helps regulate appetite, and amylin plays a role in satiation.1,4
GLP-1 is a nutrient stimulated intestinal hormone released after meals. Ghrelin is a stomach-derived hormone, leptin is an adipose-derived hormone, and both insulin and amylin are released from the pancreas in response to meals.1,7
Ghrelin stimulates hunger and promotes meal initiation. GLP-1 promotes satiety by reducing appetite and slowing gastric emptying, and it also plays a role in glucose-regulation. Leptin signals long-term energy stores and normally suppresses appetite. Insulin signals energy stores and helps regulate appetite by acting on hypothalamic pathways and reducing food reward. Amylin plays a role in satiation, glucose regulation, and bone remodeling.1,4,7
1. Apovian CM, Aronne L, Barenbaum SR. Clinical Management of Obesity. 3rd ed. Professional Communications, Inc.; 2024.
2. Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Endocrinol. 2009;2009:141753.
3. Morton GJ, Meek TH, Schwartz MW. Neurobiology of food intake in health and disease. Nat Rev Neurosci. 2014;15(6):367-378.
4. Druce MR, Small CJ, Bloom SR. Minireview: gut peptides regulating satiety. Endocrinology. 2004;145(6):2660-2665.
5. Cassidy RM, Tong Q. Hunger and satiety gauge reward sensitivity. Front Endocrinol. 2017;8:104.
6. Shah M, Vella A. Effects of GLP-1 on appetite and weight. Rev Endocr Metab Disord. 2014;15(3):181-187.
7. Hay DL, Chen S, Lutz TA, Parkes DG, Roth JD. Amylin: pharmacology, physiology, and clinical potential. Pharmacol Rev. 2015;67(3):564-600.
8. Dacquin R, Davey RA, Laplace C, et al. Amylin inhibits bone resorption while the calcitonin receptor controls bone formation in vivo. J Cell Biol. 2004;164(4):509-514.
9. Reidelberger RD, Haver AC, Arnelo U, Smith DD, Schaffert CS, Permert J. Amylin receptor blockade stimulates food intake in rats. Am J Physiol Regul Integr Comp Physiol. 2004;287(3):R568-R574. doi:10.1152
10. Gedulin BR, Rink TJ, Young AA. Dose-response for glucagonostatic effect of amylin in rats. Metabolism. 1997;46(1):67-70. doi:10.1016
11. Yamaguchi M, Watanabe Y, Ohtani T, et al. Calcitonin receptor signaling inhibits muscle stem cells from escaping the quiescent state and the niche. Cell Rep. 2015;13(2):302-314. doi:10.1016