Kelly Karen R, Brooks Latina M, Solomon Thomas P J, Kashyap Sangeeta R, O'Leary Valerie B, Kirwan John P
Department of Pathobiology, Lerner Research Institute, Cleveland, OH 44195, USA.
Am J Physiol Endocrinol Metab. 2009 Jun;296(6):E1269-74. doi: 10.1152/ajpendo.00112.2009. Epub 2009 Apr 7.
Aging and obesity are characterized by decreased beta-cell sensitivity and defects in the potentiation of nutrient-stimulated insulin secretion by GIP. Exercise and diet are known to improve glucose metabolism and the pancreatic insulin response to glucose, and this effect may be mediated through the incretin effect of GIP. The purpose of this study was to assess the effects of a 12-wk exercise training intervention (5 days/wk, 60 min/day, 75% Vo(2 max)) combined with a eucaloric (EX, n = 10) or hypocaloric (EX-HYPO, pre: 1,945 +/- 190, post: 1,269 +/- 70, kcal/day; n = 9) diet on the GIP response to glucose in older (66.8 +/- 1.5 yr), obese (34.4 +/- 1.7 kg/m(2)) adults with impaired glucose tolerance. In addition to GIP, plasma PYY(3-36), insulin, and glucose responses were measured during a 3-h, 75-g oral glucose tolerance test. Both interventions led to a significant improvement in Vo(2 max) (P < 0.05). Weight loss (kg) was significant in both groups but was greater after EX-HYPO (-8.3 +/- 1.1 vs. -2.8 +/- 0.5, P = 0.002). The glucose-stimulated insulin response was reduced after EX-HYPO (P = 0.02), as was the glucose-stimulated GIP response (P < 0.05). Furthermore, after the intervention, changes in insulin (DeltaI(0-30)/DeltaG(0-30)) and GIP (Delta(0-30)) secretion were correlated (r = 0.69, P = 0.05). The PYY(3-36) (Delta(0-30)) response to glucose was increased after both interventions (P < 0.05). We conclude that 1) a combination of caloric restriction and exercise reduces the GIP response to ingested glucose, 2) GIP may mediate the attenuated glucose-stimulated insulin response after exercise/diet interventions, and 3) the increased PYY(3-36) response represents an improved capacity to regulate satiety and potentially body weight in older, obese, insulin-resistant adults.
衰老和肥胖的特征是β细胞敏感性降低以及GIP对营养物质刺激的胰岛素分泌增强作用存在缺陷。已知运动和饮食可改善葡萄糖代谢以及胰腺对葡萄糖的胰岛素反应，并且这种作用可能是通过GIP的肠促胰岛素效应介导的。本研究的目的是评估12周运动训练干预（每周5天，每天60分钟，75%最大摄氧量）联合等热量（EX组，n = 10）或低热量（EX-HYPO组，干预前：1945±190千卡/天，干预后：1269±70千卡/天；n = 9）饮食对糖耐量受损的老年（66.8±1.5岁）肥胖（34.4±1.7千克/平方米）成年人葡萄糖刺激的GIP反应的影响。除了GIP外，还在3小时75克口服葡萄糖耐量试验期间测量了血浆PYY(3-36)、胰岛素和葡萄糖反应。两种干预均导致最大摄氧量显著改善（P < 0.05）。两组体重均显著减轻，但EX-HYPO组减重更多（-8.3±1.1千克对-2.8±0.5千克，P = 0.002）。EX-HYPO组葡萄糖刺激的胰岛素反应降低（P = 0.02），葡萄糖刺激的GIP反应也降低（P < 0.05）。此外，干预后，胰岛素（ΔI(0-30)/ΔG(0-30)）和GIP（Δ(0-30)）分泌的变化具有相关性（r = 0.69，P = 0.05）。两种干预后葡萄糖刺激的PYY(3-36)（Δ(0-30)）反应均增加（P < 0.05）。我们得出结论：1）热量限制和运动相结合可降低GIP对摄入葡萄糖的反应；2）GIP可能介导运动/饮食干预后减弱的葡萄糖刺激的胰岛素反应；3）增加的PYY(3-36)反应代表老年、肥胖、胰岛素抵抗成年人调节饱腹感及潜在体重的能力得到改善。
