Fructose and stress induce opposite effects on lipid metabolism in the visceral adipose tissue of adult female rats through glucocorticoid action.

ABSTRACT

PURPOSE: Daily exposure to stress and excessive fructose intake coincides with the growing rate of obesity and related disorders, to which women are more prone than men. Glucocorticoids, the main regulators of energy balance and response to stress, have been associated with the development of metabolic disturbances. The aim of the present study was to examine the effects of fructose overconsumption and/or chronic stress on glucocorticoid signalization and lipid metabolism in female rat adipose tissue. METHODS: We examined the effects of fructose-enriched diet and chronic unpredictable stress, separately and in combination, on glucocorticoid signaling in terms of 11ß-hydroxysteroid dehydrogenase 1 (HSD1)-catalyzed corticosterone regeneration, glucocorticoid receptor (GR) intracellular distribution, hormone binding and transcriptional regulation of genes involved in lipolysis (hormone-sensitive lipase) and lipogenesis (lipoprotein lipase, acetyl-CoA carboxylase, fatty acid synthase and phosphoenolpyruvate carboxykinase) in the visceral adipose tissue (VAT) of adult female rats. Additionally, the nuclear level of the peroxisomal proliferator-activated receptor γ (PPARγ) was analyzed. RESULTS: The combination of stress and fructose-enriched diet led to an elevation in HSD1 expression and intracellular corticosterone concentration, whereas GR nuclear accumulation was enhanced after separate treatments. Furthermore, fructose was shown to induce the expression of all examined lipogenic genes and nuclear accumulation of PPARγ, thereby stimulating adipogenesis, while stress upregulated HSL, reducing the adipose tissue mass regardless of fructose consumption. CONCLUSIONS: Prolonged overconsumption of fructose and chronic exposure to stress promote opposite effects on lipid metabolism in the VAT of adult female rats and suggest that these effects could be mediated by glucocorticoids.