title: The effects of incretins on energy homeostasis: physiology and implications for the treatment of type 2 diabetes mellitus and obesity.
abstract: Energy homeostasis in mammalians is a teleological process regulated by the interplay between caloric intake and energy expenditure. Incretins are a significant component of the complex homeostatic network regulating the metabolic state in humans. This narrative review will focus on the basic concepts regarding incretins physiology and their regulatory feedback mechanisms affecting energy homeostasis. In this context, glucagon-like peptide 1 (GLP-1) promotes satiety and weight loss through centrally and peripherally mediated pathways. On the other hand, gastric inhibitory peptide (GIP) is implicated in energy storage by its actions on adipose tissue. Understanding this biological model requires a holistic approach, since it is dually manifested by promoting weight reduction, in the case of GLP-1, or favoring lipid accumulation, in the case of GIP. The complete spectrum of incretin actions related to energy homeostasis is yet to be fully elucidated. Currently, new drugs based on incretin physiology are available for treatment of type 2 diabetes mellitus, whereas the implication of similar drugs in the treatment of obesity is under investigation. These agents exert several beneficial effects that minimize cardiovascular risk.
authors.affiliation: Unit of Reproductive Endocrinology, First Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece.
authors.forename: Spyridon
authors.initials: S
authors.lastname: Karras
authors.forename: Dimitrios G
authors.initials: DG
authors.lastname: Goulis
authors.forename: Gesthimani
authors.initials: G
authors.lastname: Mintziori
authors.forename: Niki
authors.initials: N
authors.lastname: Katsiki
authors.forename: Themistoklis
authors.initials: T
authors.lastname: Tzotzas
mesh_terms: D000818:Animals; D019440:Anti-Obesity Agents / Q000737:chemistry / Q000378:metabolism / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D015195:Drug Design; D004734:Energy Metabolism / Q000187:drug effects*; D025461:Feedback, Physiological; D006706:Homeostasis; D006801:Humans; D007004:Hypoglycemic Agents / Q000737:chemistry / Q000378:metabolism / Q000627:therapeutic use*; D054795:Incretins / Q000378:metabolism / Q000627:therapeutic use*; D009765:Obesity / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D012307:Risk Factors; D015398:Signal Transduction / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D019440:Anti-Obesity Agents; D007004:Hypoglycemic Agents; D054795:Incretins