Astrup A, Andersen T, Christensen N J, Bülow J, Madsen J, Breum L, Quaade F
Research Department of Human Nutrition, Royal Veterinary and Agricultural University, Frederiksberg, Denmark.
Am J Clin Nutr. 1990 Mar;51(3):331-7. doi: 10.1093/ajcn/51.3.331.
A reduced thermic response and an impaired activation of the sympathetic nervous system (SNS) has been reported after oral glucose in human obesity. It is, however, not known whether the reduced SNS activity returns to normal along with weight reduction. The thermic effect of glucose was lower in eight obese patients than in matched control subjects (1.7% vs 9.2%, p less than 0.002). The increase in arterial norepinephrine after glucose was also blunted in the obese patients. After a 30-kg weight loss their glucose and lipid profiles were markedly improved but the thermic effect of glucose was still lower than that of the control subjects (4.2%, p less than 0.001). The glucose-induced arterial norepinephrine response remained diminished in the reduced obese patients whereas the changes in plasma epinephrine were similar in all three groups. The results suggest that a defective SNS may be a cause in the development of obesity.
据报道，人类肥胖症患者口服葡萄糖后，热反应降低，交感神经系统（SNS）激活受损。然而，尚不清楚SNS活性降低是否会随着体重减轻而恢复正常。8名肥胖患者的葡萄糖热效应低于匹配的对照受试者（1.7%对9.2%，p<0.002）。肥胖患者口服葡萄糖后动脉去甲肾上腺素的增加也减弱。体重减轻30公斤后，他们的血糖和血脂谱明显改善，但葡萄糖热效应仍低于对照受试者（4.2%，p<0.001）。体重减轻的肥胖患者中，葡萄糖诱导的动脉去甲肾上腺素反应仍然减弱，而三组患者血浆肾上腺素的变化相似。结果表明，SNS功能缺陷可能是肥胖症发生的一个原因。
