Valensi P, Lormeau B, Dabbech M, Miossec P, Pariès J, Dauchy F, Attali J R
Department of Endocrinology-Diabetology-Nutrition, Jean Verdier Hospital, Paris-Nord University, Bondy, France.
Int J Obes Relat Metab Disord. 1998 Jun;22(6):494-9. doi: 10.1038/sj.ijo.0800609.
The aim of this study was to look for a relationship between autonomic dysfunction and alterations in glucose- induced thermogenesis (GIT) and lipid oxidation rate in obese non-diabetic women.
37 obese women, 20 with impaired cardiac autonomic function tests (group 1) were matched with 17 women with normal tests (group 2) according to age, weight, body mass index (BMI), waist-to-hip ratio (WHR), fat mass (FM) and fat free mass (FFM).
A series of five standardized tests was carried out, three of which were based mainly on cardiac parasympathetic control (heart rate response to Valsalva, deep breathing and lying-to-standing) and two on cardiovascular sympathetic function (blood pressure response to standing and to handgrip). Energy expenditure (EE), lipid and glucose oxidation rate were determined by indirect calorimetry at fasting and after an oral glucose load (75 g). Blood glucose, insulin and catecholamines responses to glucose were examined.
There was no significant difference in plasma glucose, insulin, catecholamines, metabolic rate, glucose and lipid oxidation rate at fasting and plasma glucose, insulin and catecholamine responses to glucose. GIT was slightly but not significantly lower in group 1 (24.7+/-10.4 kJ) than in group 2 (46.8+/-9.0 kJ). The cumulative glucose oxidation rate did not differ significantly in the two groups. The cumulative lipid oxidation rate was significantly lower in group 1 than in group 2 (-49.4+/-4.1 vs -30.8+/-8.0, respectively, P = 0.033). It correlated negatively with the area under the curve of insulin response (r=-0.37, P=0.04). In the multivariate analysis, both autonomic dysfunction and the area under the curve of insulin response correlated significantly with the cumulative lipid oxidation rate.
This study suggests that 1) the glucose-induced inhibition of the lipid oxidation rate in obese women is greater in the patients with autonomic dysfunction; 2) a decrease in sympathetic activity is likely to be involved in this phenomenon.
本研究旨在探寻肥胖非糖尿病女性自主神经功能障碍与葡萄糖诱导的产热（GIT）及脂质氧化率改变之间的关系。
37名肥胖女性，其中20名心脏自主神经功能测试受损者（第1组）与17名测试正常的女性（第2组）根据年龄、体重、体重指数（BMI）、腰臀比（WHR）、脂肪量（FM）和去脂体重（FFM）进行匹配。
进行了一系列五项标准化测试，其中三项主要基于心脏副交感神经控制（对瓦尔萨尔瓦动作、深呼吸和卧位到立位的心率反应），两项基于心血管交感神经功能（对站立和握力的血压反应）。通过间接测热法测定空腹及口服葡萄糖负荷（75克）后的能量消耗（EE）、脂质和葡萄糖氧化率。检测血糖、胰岛素和儿茶酚胺对葡萄糖的反应。
空腹时血浆葡萄糖、胰岛素、儿茶酚胺、代谢率、葡萄糖和脂质氧化率以及血浆葡萄糖、胰岛素和儿茶酚胺对葡萄糖的反应在两组间无显著差异。第1组的GIT（24.7±10.4千焦）略低于第2组（46.8±9.0千焦），但差异不显著。两组的累积葡萄糖氧化率无显著差异。第1组的累积脂质氧化率显著低于第2组（分别为-49.4±4.1与-30.8±8.0，P = 0.033）。它与胰岛素反应曲线下面积呈负相关（r = -0.37，P = 0.04）。在多变量分析中，自主神经功能障碍和胰岛素反应曲线下面积均与累积脂质氧化率显著相关。
本研究表明，1）自主神经功能障碍患者中，肥胖女性葡萄糖诱导的脂质氧化率抑制作用更强；2）交感神经活动降低可能与这一现象有关。
