Estrogens and glucocorticoid hormones in adipose tissue metabolism.

@article{citeulike:2229876, abstract = {Women have a higher percentage of body fat than men, and there is a gender-specific difference in fat distribution: Females tend to accumulate fat around the hips, buttocks, and thighs while men have a larger intra-abdominal (visceral) fat mass. After menopause, there is a redistribution of fat depots, and post-menopausal women develop increased amounts of visceral fat. The risk of developing obesity-related diseases is significantly lower in pre-menopausal women compared to men, a difference that is abolished after menopause, suggesting that the female sex steroid estrogen influences adipogenesis and adipose metabolism. Experimentally, estrogen increases the size and number of subcutaneous adipocytes and attenuates lipolysis. Post-menopausal women also develop a more atherogenic lipid pattern and decreased levels of the prothrombotic protein plasminogen activator inhibitor-1, which attenuates fibrinolysis. Pathologically increased circulating cortisol concentration is associated with dysmetabolic features e.g., central obesity, elevated blood pressure, insulin resistance, and dyslipidemia. In "simple obesity," glucocorticoid production is elevated. Peak levels of circulating cortisol are however low or normal, possibly because of increased clearance and/or tissue-specific changes in cortisol production. In addition to the adrenal production of cortisol, cortisol is also generated in adipose tissue by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) which converts inactive cortisone to active cortisol. The enzyme activity in subcutaneous fat increases with increasing body weight. Estrogen seems to have a tissue-specific influence on 11betaHSD1 enzyme activity, attenuating it in liver, kidney, and testis but upregulating 11betaHSD1 mRNA expression in preadipocytes from women. In the present review, we summarize and discuss the interaction between glucocorticoids and sex steroids and their influence on adipocyte metabolism.}, address = {Department of Medicine and Public Health, Ume\r{a} University Hospital, Ume\r{a}, Sweden. cecilia.mattsson@medicin.umu.se.}, author = {Mattsson, C. and Olsson, T. }, citeulike-article-id = {2229876}, issn = {0929-8673}, journal = {Curr Med Chem}, keywords = {adipose, estrogens, glucocorticoids, review}, number = {27}, pages = {2918--2924}, posted-at = {2008-01-14 10:44:05}, priority = {2}, title = {Estrogens and glucocorticoid hormones in adipose tissue metabolism.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/18045137}, volume = {14}, year = {2007} }

TY - JOUR ID - citeulike:2229876 L3 - citeulike-article-id:2229876 TI - Estrogens and glucocorticoid hormones in adipose tissue metabolism. JF - Curr Med Chem VL - 14 IS - 27 SP - 2918 EP - 2924 AD - Department of Medicine and Public Health, Umeå University Hospital, Umeå, Sweden. cecilia.mattsson@medicin.umu.se. SN - 0929-8673 N2 - Women have a higher percentage of body fat than men, and there is a gender-specific difference in fat distribution: Females tend to accumulate fat around the hips, buttocks, and thighs while men have a larger intra-abdominal (visceral) fat mass. After menopause, there is a redistribution of fat depots, and post-menopausal women develop increased amounts of visceral fat. The risk of developing obesity-related diseases is significantly lower in pre-menopausal women compared to men, a difference that is abolished after menopause, suggesting that the female sex steroid estrogen influences adipogenesis and adipose metabolism. Experimentally, estrogen increases the size and number of subcutaneous adipocytes and attenuates lipolysis. Post-menopausal women also develop a more atherogenic lipid pattern and decreased levels of the prothrombotic protein plasminogen activator inhibitor-1, which attenuates fibrinolysis. Pathologically increased circulating cortisol concentration is associated with dysmetabolic features e.g., central obesity, elevated blood pressure, insulin resistance, and dyslipidemia. In "simple obesity," glucocorticoid production is elevated. Peak levels of circulating cortisol are however low or normal, possibly because of increased clearance and/or tissue-specific changes in cortisol production. In addition to the adrenal production of cortisol, cortisol is also generated in adipose tissue by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) which converts inactive cortisone to active cortisol. The enzyme activity in subcutaneous fat increases with increasing body weight. Estrogen seems to have a tissue-specific influence on 11betaHSD1 enzyme activity, attenuating it in liver, kidney, and testis but upregulating 11betaHSD1 mRNA expression in preadipocytes from women. In the present review, we summarize and discuss the interaction between glucocorticoids and sex steroids and their influence on adipocyte metabolism. KW - adipose KW - estrogens KW - glucocorticoids KW - review AU - Mattsson, C AU - Olsson, T PY - 2007/// UR - http://view.ncbi.nlm.nih.gov/pubmed/18045137 ER -