Endurance exercise training increases adipose tissue glucocorticoid exposure: adaptations that facilitate lipolysis
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abstract
Glucocorticoids (GCs) have long been thought to be lipolytic in nature. Recently, however, increased exposure to GCs in insulin-sensitive tissues has been associated with lipid accumulation and metabolic complications, regardless of plasma concentrations. Intracellular GC action is determined by both 11-beta hydroxysteroid dehydrogenase type 1 (11betaHSD1) and the GC receptor (GR). We hypothesized that exercise training would increase 11betaHSD1 and GR protein in adipose tissue, resulting in increased lipolysis. To test the effects of exercise on adipose tissue GR and 11betaHSD1 protein, 2 sets of hamsters were trained for 6 weeks: young, diet-induced obese animals and older, overweight animals. Young (6 week old) hamsters, fructose-fed to induce an obese phenotype, and older (6 month old) hamsters were randomly divided into exercising and sedentary groups. Exercise training decreased adipose tissue mass in both fructose-fed and older hamsters. In addition, exercise training increased 11betaHSD1 (31.5% +/- 15% and 20.0% +/- 7%, fructose-fed and older, respectively) and GR (45.6% +/- 14% and 61.1% +/- 27%, fructose-fed and older, respectively) protein expression in the perirenal adipose depot and increased 11betaHSD1 (16.7% +/- 7%, P = .09) and GR (47.4% +/- 19%, P < .05) in the subcutaneous adipose depot of the older hamsters. To determine the metabolic effect of increased GC exposure in adipocytes, 3T3-L1 adipocytes were treated with corticosterone for 24 hours; and measures of lipolytic rates were conducted. Low concentrations of GCs (0.01-0.1 micromol/L) increased GR (44.1% +/- 18%, P < .05) and 11betaHSD1 (95.3% +/- 24%) protein expression, as well as lipolytic rates (34.6% +/- 6%) as measured by glycerol release. The increased lipolysis was blocked by RU486, a GR antagonist, suggesting that the elevated lipolysis was a direct result of GC action. These results suggest that exercise training amplifies the activity of GCs in adipose tissue of overweight animals through alterations in 11betaHSD1 and GR despite differences in age and amounts of adiposity. In vitro, GCs are capable of increasing lipolysis, but depend upon the presence of GR. We propose that GCs play a significant role in changing the phenotype of adipose tissue during exercise training, resulting in decreased fat mass.
