期刊
OBESITY
卷 22, 期 6, 页码 1477-1484出版社
WILEY-BLACKWELL
DOI: 10.1002/oby.20719
关键词
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资金
- National Institutes of Health [P50 HD044405, RO1 DK074970-01]
- March of Dimes [6-FY07-678]
- American Heart Association [11IRG5570010]
- American Diabetes Association [7-13-BS-101]
Objective Androgen excess in women is associated with visceral adiposity. However, little is known on the mechanism through which androgen promotes visceral fat accumulation. Methods To address this issue, female mice to chronic androgen excess using 5-dihydrotestosterone (DHT) and studied the regulation of energy homeostasis was exposed. Results DHT induced a leptin failure to decrease body weight associated with visceral adiposity but without alterations in leptin anorectic action. This paralleled leptin's failure to upregulate brown adipose tissue expression of uncoupling protein-1, associated with decreased energy expenditure (EE). DHT decreased hypothalamic proopiomelanocortin (pomc) mRNA expression and increased POMC intensity in neuronal bodies of the arcuate nucleus while simultaneously decreasing the intensity of POMC projections to the dorsomedial hypothalamus (DMH). This was associated with a failure of the melanocortin 4 receptor agonist melanotan-II to suppress body weight. Conclusion Taken together, these data indicate that androgen excess promotes visceral adiposity with reduced POMC neuronal innervation in the DMH, reduced EE but without hyperphagia.
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