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OBJECTIVE: 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. SUBJECTS: 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). MEASUREMENTS: A series of ®ve 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. RESULTS: There was no signi®cant 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 signi®cantly lower in group 1 (24.7 AE 10.4 kJ) than in group 2 (46.8 AE 9.0 kJ). The cumulative glucose oxidation rate did not differ signi®cantly in the two groups. The cumulative lipid oxidation rate was signi®cantly lower in group 1 than in group 2 (749.4 AE 4.1 vs 730.8 AE 8.0, respectively, P 0.033). It correlated negatively with the area under the curve of insulin response (r 70.37, P 0.04). In the multivariate analysis, both autonomic dysfunction and the area under the curve of insulin response correlated signi®cantly with the cumulative lipid oxidation rate. CONCLUSION: 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.

Fifty adult female Swiss albino mice were injected with either 1.11 mg/kg body weight pyridoxine or saline, subsequently they were all submitted to an immobilization stress with a complete fast for 17 h. At the end of this period, the animals were sacrificed, the gastric mucosa was dissected for ulcer count, and brain noradrenaline, dopamine and serotonin were determined by liquid chromatography. In addition, 26 non stressed mice were used as controls, 16 of them being fed at libitum and 10 submitted to the same fasting period as the first two groups. In the stressed animals, the average number of gastric ulcers per mouse was twice as large in the saline-treated group than in the pyridoxine-treated group (p < 0.05). With a single exception, no ulcer was found in the non stressed controls. Brain norepinephrine content was almost identical in fasting controls and in stressed mice treated with pyridoxine; in the stressed animals treated with saline, the average norepinephrine content was higher by 15 % and in the fed controls lower by 11 % than in the two preceding groups. Pyridoxine treatment entailed a very significant reduction (p < 0.002) of norepinephrine variability, mainly due to the absence of high values (≧ 750 ng/g of fresh brain) which occurred only in the saline-treated group. Similar results were yielded for brain dopamine. No variations were observed for brain serotonin. These results suggest the antistress effect of pyridoxine.