Brown adipose tissue remodeling induced by corticosterone in Wistar male rats

New Findings

What is the central question of this study?

Brown adipose tissue is centrally involved in energy metabolism. The aim of this work was to test the hypothesis that glucocorticoids excess disrupts BAT phenotype and function.

What is the main finding and its importance?

This work highlights that glucocorticoids might be an important modulator of brown fat physiology. Furthermore, it suggests a role for brown adipose tissue on pathophysiology of metabolic disturbances induced by glucocorticoid excess.

Abstract

In mammals, brown adipose tissue (BAT) is centrally involved in energy metabolism. To test the hypothesis that glucocorticoids excess disrupts BAT phenotype and function, male Wistar rats were treated with corticosterone in drinking water for 21 days. To confirm induction of glucocorticoid excess and metabolic disturbances, adrenals weight, corticotrophin releasing hormone mRNA levels, corticosterone serum levels, glucose tolerance test and serum triacylglycerol analyses were performed. Adipose tissue deposits were excised, weighed and evaluated by a set of biochemical, histological and molecular procedures, such as: thin‐layer chromatography, histochemistry, immunohistochemistry, quantitative real‐time polymerase chain reaction, high‐resolution oxygraphy, ATP synthesis and enzymatic activity measurements. The approach was successful in induction of glucocorticoid excess and metabolic disturbances. Lower body weight and increased adiposity were observed in corticosterone‐treated rats. Interscapular brown adipose tissue (iBAT) showed higher sensitivity to glucocorticoids than other fat deposits. The treatment induced lipid accumulation, unilocular rearrangement, increased collagen content and decreased innervation in iBAT. Furthermore, expression of Prdm16 (P < 0.05), Ucp1 (P < 0.05) and Slc7a10 (P < 0.05) decreased, while expression of Fasn (P < 0.05) and Lep (P < 0.05) mRNA increased in brown adipose tissue. Also, the levels of UCP1 diminished (P < 0.001, 2.5‐fold). Finally, lower oxygen consumption (P < 0.05), ATP synthesis (P < 0.05) and mitochondrial content (P < 0.05) were observed in iBAT of GCs‐treated rats. Glucocorticoid excess induced an extensive remodeling of interscapular brown adipose tissue, resulting in a white‐like phenotype in association with metabolic disturbances.

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