Changes in tumor necrosis factor-alpha system and insulin sensitivity during an exercise training program in obese women with normal and impaired glucose tolerance.

OBJECTIVE: Tumor necrosis factor-alpha (TNFalpha) plays an important role in the pathogenesis of insulin resistance and type 2 diabetes. Plasma levels of the soluble (s) fractions of TNFalpha receptors, especially sTNFR2, are good indicators of TNFalpha system activation in obesity. The aim of the present study was to assess the effect of exercise training on the TNFalpha system and to evaluate the relationship with changes in insulin sensitivity. DESIGN AND METHODS: Sixteen obese women (body mass index (BMI)>27.8 kg/m(2)), 8 with normal (NGT) and 8 with impaired glucose tolerance (IGT), participated in an exercise training program which lasted for 12 weeks and included exercise performed on a bicycle ergometer at an individual intensity of 70% maximal heart rate, for 30 min, 5 days a week. Anthropometrical measurements and blood biochemical analyses were performed, and plasma TNFalpha, sTNFR1 and sTNFR2 levels were assessed. Insulin sensitivity was evaluated using the hyperinsulinemic euglycemic clamp technique (insulin infusion: 50 mU x kg(-1)xh(-1)). RESULTS: At baseline, despite similar anthropometrical parameters, IGT subjects were markedly more insulin resistant and had higher TNFalpha and sTNFR2 concentrations. Exercise training increased insulin sensitivity and decreased TNFalpha and sTNFR2 levels, while sTNFR1 remained unchanged. The decrease in sTNFR2 was significantly related to the increase in insulin sensitivity; that relationship remained significant after adjustment for the concurrent changes in BMI, waist circumference, percentage of body fat, plasma glucose, insulin and free fatty acids. CONCLUSIONS: Regular physical exercise decreases TNFalpha system activity and that decrease may be responsible for the concurrent increase in insulin sensitivity.

The effect of exercise training on glucose tolerance and skeletal muscle triacylglycerol content in rats fed with a high-fat diet.

The aim of the present study was to evaluate the effect of exercise training on glucose tolerance and glycogen and triacylglycerol (TG) content in different types of skeletal muscles and in the liver of rats fed with a high-fat diet. From 8 to 11 weeks of age male Wistar rats were fed with isocaloric standard (control) or high-fat diet (HFD--59% calories as fat) and were additionally assigned to a sedentary or trained group (4 weeks of training on a treadmill). An intravenous glucose tolerance test (IVGTT) with the determination of basal and post load insulin was performed before the final tissue sampling. HFD rats developed marked hyperinsulinemia. Exercise training improved glucose tolerance and insulin response in the control group only (AUC for glucose in control sedentary vs control trained, p<0.05; AUC for insulin: control sedentary vs control trained, p<0.005). Liver glycogen was significantly lower in the HFD group (p<0.05 vs control sedentary) and did not increase after exercise training. Muscle and liver TG content was markedly higher in the HFD group in comparison to control (p<0.0001 in all cases). Exercise training increased TG content in the control group in all examined tissues except white gastrocnemius (p<0.001 in all cases compared to sedentary controls), and did not affect tissue TG in the HFD group. After exercise training there was still markedly higher tissue TG content in the HFD group vs control (p<0.0001 in all cases). We conclude that beneficial metabolic effects of training are impaired in high-fat fed rats and that training does not completely reverse metabolic disturbances in this group of animals.