Verga S, Buscemi S, Bompiani G
University of Palermo, Istituto di Clinica Medica, Policlinico P. Giaccone, Italy.
Eur J Clin Nutr. 1990 May;44(5):397-404.
In order to assess to what extent familial factors play a role in thermogenesis of obese individuals, the 3 h response to a 100 g glucose oral load was measured in 11 obese subjects (6 m, 5 f) with a familial history of obesity and/or obesity-non-insulin dependent diabetes mellitus (NIDDM, group A); these were compared to 9 obese subjects (5 m, 4 f) without familial history of these disorders (group B). All subjects had normal glucose tolerance and the two groups were comparable with respect to anthropometric features. The glucose-induced thermogenesis of group A (7.9 +/- 1.2 per cent) above preload energy expenditure was significantly lower (P less than 0.01) than that observed in group B (13.5 +/- 0.5 per cent). The same conclusions were obtained when the results were expressed as a percentage of the glucose load ingested (4.4 +/- 0.67 and 7.8 +/- 0.80 in group A and group B respectively, P less than 0.01). Despite these differences the pattern of change in glycaemia, insulinaemia, C-peptidaemia and glucagonaemia in response to the glucose load was the same between the two groups. Total glucose oxidation as well as non-oxidative glucose disposal did not differ between the two groups. These results seem to support the hypothesis that genetic factors may contribute to the low thermogenic response observed in some individuals with a familial history of obesity and/or obesity-NIDDM.
为了评估家族因素在肥胖个体产热过程中所起的作用程度，对11名有肥胖和/或肥胖型非胰岛素依赖型糖尿病（NIDDM，A组）家族史的肥胖受试者（6名男性，5名女性）进行了口服100克葡萄糖后3小时的反应测量；将这些受试者与9名无上述疾病家族史的肥胖受试者（5名男性，4名女性）（B组）进行比较。所有受试者糖耐量均正常，两组在人体测量特征方面具有可比性。A组葡萄糖诱导的产热（高于负荷前能量消耗的7.9±1.2%）显著低于B组（13.5±0.5%）（P<0.01）。当结果以摄入葡萄糖负荷的百分比表示时，也得出了相同的结论（A组和B组分别为4.4±0.67和7.8±0.80，P<0.01）。尽管存在这些差异，但两组对葡萄糖负荷的血糖、胰岛素血症、C肽血症和胰高血糖素血症的变化模式是相同的。两组之间的总葡萄糖氧化以及非氧化葡萄糖处理没有差异。这些结果似乎支持了这样一种假设，即遗传因素可能导致在一些有肥胖和/或肥胖型NIDDM家族史的个体中观察到的低产热反应。
