Running exercise increases tumor necrosis factor-α secreting from mesenteric fat in insulin-resistant rats

Tumor necrosis factor-α (TNF-α) is an important mediator of insulin resistance in obese subjects, through its overexpression in fat tissue. However, how exercise can modify the expression of TNF-α is controversial. We examined TNF-α in adipose tissue using an animal model of insulin resistance that was produced by feeding rats a diet high in sucrose. The rats were allocated to one of three groups: those receiving a starch-based diet (control group): those fed a high-sucrose diet (sucrose-fed group): and those fed a high-sucrose diet and given wheel exercise (exercised group). The animals were allowed to eat and drink ad lib for 4 or 12 weeks (4 wk: control n = 7, sucrose-fed n = 7, exercised n = 10; 12 wk: control n = 5, sucrose-fed n = 5, exercised n = 9). The voluntary wheel exercise was initiated with the feeding of the high-sucrose diet. The rats in the exercise groups ran 15 ± 3 km week . We showed that 12-week voluntary running exercise significantly (P < 0.05) increased both TNF-α protein (5-fold) and mRNA (1.4 fold) in the mesenteric fat of insulin-resistant rats compared to non-exercised sucrose-fed mice. Accordingly, in exercised group, plasma glucose (124 ± 9 Eq L vs 141 ± 11 Eq L ) and free fatty acid (0.98 ± 0.07 Eq L vs 1.4 ± 0.05 mEq L ) concentrating in portal vein blood were reduced compared to sucrose-fed group. The amounts of fatty tissue both in mesenteric and subcutaneous tissues were significantly (P < 0.05) decreased through running exercise. We consider that up-regulation of TNF-α in mesenteric fat may be a compensatory mechanism for the reduction of fatty acid in adipose tissues and this change could control metabolic homeostasis during exercise to modulate a hyperinsulinemic state.