Golay A, Jallut D, Schutz Y, Felber J P, Jéquier E
Department of Internal Medicine, Lausanne University Hospital, Switzerland.
Int J Obes. 1991 Sep;15(9):601-7.
The thermogenic response to a 100 g oral glucose load was measured prospectively (by indirect calorimetry) in three groups of obese subjects: (1) normal glucose tolerance (n = 12, initial weight 86.4 +/- 3.9 kg, BMI 30.4 +/- 1.1 kg/m2; (2) impaired glucose tolerance (n = 8, initial weight 105.3 +/- 7.6 kg, body mass index (BMI) 37.6 +/- 2.9 kg/m2; (3) diabetes (n = 12), initial weight 102.1 +/- 5.3 kg, BMI 36.2 +/- 2.0 kg/m2). The thermogenic response to glucose averaged 6.8 +/- 1.1 and 7.0 +/- 1.0 per cent, in the two non-diabetic obese groups respectively, and was significantly lower in the obese diabetic group (3.1 +/- 0.8 per cent). With the evolution of obesity (i.e. 6 years later), the glucose-induced thermogenesis (GIT) was significantly reduced in the non-diabetic groups (P less than 0.05) to 4.1 +/- 0.8 and 3.0 +/- 1.1 per cent respectively, and was still blunted in the diabetic group (2.1 +/- 0.7 per cent). The decrease in GIT was accompanied by a reduction in glucose tolerance and insulin response with no change in fasting plasma insulin. These effects were observed despite the fact that the body weight of the subject did not change significantly over the 6-year period. It is concluded that the decrease in GIT which accompanies the worsening of glucose tolerance and the occurrence of diabetes is a mechanism which may contribute to maintain the obesity state by a reduction of energy expenditure.
通过间接测热法对三组肥胖受试者口服100克葡萄糖后的产热反应进行了前瞻性测量：（1）糖耐量正常组（n = 12，初始体重86.4±3.9千克，体重指数（BMI）30.4±1.1千克/平方米）；（2）糖耐量受损组（n = 8，初始体重105.3±7.6千克，体重指数（BMI）37.6±2.9千克/平方米）；（3）糖尿病组（n = 12），初始体重102.1±5.3千克，BMI 36.2±2.0千克/平方米）。两个非糖尿病肥胖组对葡萄糖的产热反应平均分别为6.8±1.1%和7.0±1.0%，而肥胖糖尿病组显著更低（3.1±0.8%）。随着肥胖的进展（即6年后），非糖尿病组中葡萄糖诱导的产热（GIT）显著降低（P<0.05），分别降至4.1±0.8%和3.0±1.1%，糖尿病组仍受到抑制（2.1±0.7%）。GIT的降低伴随着糖耐量和胰岛素反应的降低，而空腹血浆胰岛素无变化。尽管受试者的体重在6年期间没有显著变化，但仍观察到了这些效应。结论是，伴随着糖耐量恶化和糖尿病发生的GIT降低是一种可能通过减少能量消耗来维持肥胖状态的机制。
