Department of Pathobiology, Lerner Research Institute and Nutrition, Case Western Reserve University, Cleveland, OH, USA.
Am J Clin Nutr. 2010 Dec;92(6):1359-68. doi: 10.3945/ajcn.2010.29771. Epub 2010 Oct 27.
The optimal lifestyle intervention that reverses diabetes risk factors is not known.
We examined the effect of a low-glycemic index (GI) diet and exercise intervention on glucose metabolism and insulin secretion in obese, prediabetic individuals.
Twenty-two participants [mean ± SEM age: 66 ± 1 y; body mass index (in kg/m(2)): 34.4 ± 0.8] underwent a 12-wk exercise-training intervention (1 h/d for 5 d/wk at ≈ 85% of maximum heart rate) while randomly assigned to receive either a low-GI diet (LoGIX; 40 ± 0.3 units) or a high-GI diet (HiGIX; 80 ± 0.6 units). Body composition (measured by using dual-energy X-ray absorptiometry and computed tomography), insulin sensitivity (measured with a hyperinsulinemic euglycemic clamp with [6,6-(2)H(2)]-glucose), and oral glucose-induced insulin and incretin hormone secretion were examined.
Both groups lost equal amounts of body weight (-8.8 ± 0.9%) and adiposity and showed similar improvements in peripheral tissue (+76.2 ± 14.9%) and hepatic insulin sensitivity (+27.1 ± 7.1%) (all P < 0.05). However, oral glucose-induced insulin secretion was reduced only in the LoGIX group (6.59 ± 0.86 nmol in the prestudy compared with 4.70 ± 0.67 nmol in the poststudy, P < 0.05), which was a change related to the suppressed postprandial response of glucose-dependent insulinotropic polypeptide. When corrected for changes in β cell glucose exposure, changes in insulin secretion were attenuated in the LoGIX group but became significantly elevated in the HiGIX group.
Although lifestyle-induced weight loss improves insulin resistance in prediabetic individuals, postprandial hyperinsulinemia is reduced only when a low-GI diet is consumed. In contrast, a high-GI diet impairs pancreatic β cell and intestinal K cell function despite significant weight loss. These findings highlight the important role of the gut in mediating the effects of a low-GI diet on type 2 diabetes risk reduction.
目前尚不清楚哪种生活方式干预最有利于逆转糖尿病的危险因素。
本研究旨在探讨低血糖生成指数(GI)饮食和运动干预对肥胖、糖尿病前期个体葡萄糖代谢和胰岛素分泌的影响。
22 名参与者(平均年龄 ± SEM:66 ± 1 岁;体重指数(kg/m2):34.4 ± 0.8)接受了 12 周的运动训练干预(每天 1 小时,每周 5 天,约为最大心率的 85%),并随机分为接受低血糖生成指数饮食(LoGIX;40 ± 0.3 单位)或高血糖生成指数饮食(HiGIX;80 ± 0.6 单位)组。通过双能 X 射线吸收法和计算机断层扫描测量身体成分,用高胰岛素-正葡萄糖钳夹技术(用[6,6-(2)H2]-葡萄糖)检测胰岛素敏感性,口服葡萄糖后检测胰岛素和肠促胰岛素激素的分泌情况。
两组的体重(-8.8 ± 0.9%)和体脂量均等量下降,外周组织(+76.2 ± 14.9%)和肝脏胰岛素敏感性(+27.1 ± 7.1%)均得到类似改善(均 P < 0.05)。然而,仅在 LoGIX 组中观察到口服葡萄糖诱导的胰岛素分泌减少(在研究前为 6.59 ± 0.86 nmol,研究后为 4.70 ± 0.67 nmol,P < 0.05),这与餐后胰高血糖素样肽 1 的反应受抑制有关。当校正β细胞葡萄糖暴露的变化时,LoGIX 组的胰岛素分泌变化减弱,但 HiGIX 组的胰岛素分泌变化显著升高。
尽管生活方式引起的体重减轻改善了糖尿病前期个体的胰岛素抵抗,但只有在摄入低血糖生成指数饮食时,才会降低餐后高胰岛素血症。相反,尽管体重显著减轻,高血糖生成指数饮食仍会损害胰岛β细胞和肠道 K 细胞的功能。这些发现强调了肠道在介导低血糖生成指数饮食对 2 型糖尿病风险降低的作用中的重要性。