Steinert Robert E, Feinle-Bisset Christine, Asarian Lori, Horowitz Michael, Beglinger Christoph, Geary Nori
University of Adelaide Discipline of Medicine and National Health and Medical Research Council of Australia Centre of Research Excellence in Translating Nutritional Science to Good Health, Adelaide, Australia; DSM Nutritional Products, R&D Human Nutrition and Health, Basel, Switzerland; Institute of Veterinary Physiology, University of Zurich, Zurich, Switzerland; Department of Biomedicine and Division of Gastroenterology, University Hospital Basel, Basel, Switzerland; and Department of Psychiatry, Weill Medical College of Cornell University, New York, New York.
Physiol Rev. 2017 Jan;97(1):411-463. doi: 10.1152/physrev.00031.2014.
The efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3-36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3-36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3-36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.
Roux-en-Y胃旁路术（RYGB）及其他减肥手术在肥胖症和2型糖尿病治疗中的疗效，以及胃肠（GI）内分泌学的新进展，重新引发了人们对胃肠激素在饮食控制、进餐相关血糖及肥胖症中作用的兴趣。在此，我们综述了控制四种此类激素（胃饥饿素、胆囊收缩素（CCK）、胰高血糖素样肽-1（GLP-1）和酪酪肽[PYY(3-36)]）分泌的营养感知机制，以及它们对健康体重者、肥胖者及RYGB患者胃肠运动功能、食物摄入和进餐相关血糖升高控制的贡献。讨论了它们作为经典内分泌信号和局部作用信号的生理作用。胃排空、小肠肠内分泌细胞对特定消化产物的检测以及不同胃肠位点之间的协同相互作用均有助于胃饥饿素、CCK、GLP-1和PYY(3-36)的分泌。虽然CCK已被充分确认为健康体重者饮食的内源性内分泌控制因素，但这四种激素在肥胖者饮食及RYGB术后的作用尚不确定。同样，只有GLP-1明显有助于进餐相关血糖的内分泌控制。这些激素的作用可能涉及局部信号传导，但缺乏确定局部信号传导效应生理状态的方法。需要进一步研究和新方法来更好地理解胃饥饿素、CCK、GLP-1和PYY(3-36)的生理学；它们在肥胖症和减肥手术中的作用；以及它们的治疗潜力。
