首页> 外文期刊>European journal of clinical nutrition >Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight.
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Postprandial insulin response and mitochondrial oxidation in obese men nutritionally treated to lose weight.

机译:营养治疗减肥的肥胖男性的餐后胰岛素反应和线粒体氧化。

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摘要

Obesity, hyperglycemia, and insulin resistance have been associated to an oxidative mitochondrial dysfunction. The aim of this research was to evaluate the relation between carbohydrate metabolism and mitochondrial oxidation, as affected by the weight status and the weight loss induced by a calorie-restricted diet. Lean control men (BMI<25 kg/m2, n = 6) and obese men (BMI>30 kg/m2, n = 14), who were characterized as insulin resistant (n = 6) or insulin sensitive (n = 8) based on HOMA index values, participated in the trial. Plasma insulin levels and mitochondrial oxidation estimated by the 2-keto(1-13C)isocaproate breath test, were measured after ingestion of a test meal during 3 h. Obese subjects repeated the breath test protocol after a 10-week caloric restriction diet to lose weight. Postprandial insulin secretion tended to be marginally higher (P = 0.059) in both obese groups than in controls, while the rate of postprandial mitochondrial oxidation was markedly decreased (P = 0.019) in the obese subjects as compared with lean individuals. The nutritionally induced weight loss produced a rise in the postprandial oxidative process in volunteers initially considered as insulin resistant (P = 0.036), while no statistical differences in the insulin-sensitive obese (P = 0.241) were found. Interestingly, the percentage of oxidized tracer was inversely related to postprandial insulin secretion (r = -0.56; P = 0.001). In conclusion, these results support the hypothetized relation between carbohydrate metabolism and mitochondrial oxidation at a postprandial state in obese subjects, raising interest about mitochondria stimulation as a target in the therapy of obesity.
机译:肥胖,高血糖和胰岛素抵抗已与氧化线粒体功能障碍有关。这项研究的目的是评估受体重限制和低热量饮食引起的体重减轻影响的碳水化合物代谢与线粒体氧化之间的关系。精瘦对照男性(BMI <25 kg / m2,n = 6)和肥胖男性(BMI> 30 kg / m2,n = 14),其特征为胰岛素抵抗(n = 6)或胰岛素敏感(n = 8)根据HOMA指数值,参加了试验。在3小时内摄入试验餐后,通过2-酮(1-13C)异己酸呼气试验评估了血浆胰岛素水平和线粒体氧化。肥胖受试者在限制饮食10周以减肥后,重复了呼气试验规程。与瘦人相比,两个肥胖组的餐后胰岛素分泌往往比对照组略高(P = 0.059),而肥胖受试者的餐后线粒体氧化率显着降低(P = 0.019)。营养诱发的体重减轻最初被认为是胰岛素抵抗的志愿者的餐后氧化过程增加(P = 0.036),而对胰岛素敏感的肥胖者没有统计学差异(P = 0.241)。有趣的是,氧化示踪剂的百分比与餐后胰岛素分泌呈负相关(r = -0.56; P = 0.001)。总之,这些结果支持了肥胖受试者餐后状态下碳水化合物代谢与线粒体氧化之间的假想关系,引起了人们对将线粒体刺激作为肥胖症治疗目标的兴趣。

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