Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism

• Published in: Current medicinal chemistry Vol. 14; no. 27; pp. 2918 - 2924
• Main Authors: MATTSSON, Cecilia, OLSSON, Tommy
• Format: Journal Article
• Language: English
• Published: Schiphol Bentham Science Publishers Ltd 01.11.2007; Bentham Science
• Subjects: Adiponectin - physiology; Adipose tissue; Adipose Tissue - metabolism; Animals; Biological and medical sciences; Blood pressure; Body fat; Body weight; Dehydrogenase; Enzymatic activity; Estrogens; Estrogens - physiology; Female; Females; Fundamental and applied biological sciences. Psychology; Gender; Glucocorticoids - physiology; Hormones; Humans; Hydrocortisone - metabolism; Hypertension; Inflammation - metabolism; Insulin - metabolism; Kidneys; Leptin - physiology; Lipid Metabolism; Lipids. Glycolipids; Male; Medical sciences; Menopause; Metabolic diseases; Metabolisms and neurohumoral controls; Miscellaneous; Obesity; Other metabolic disorders; Receptors, Estrogen - physiology; Steroids; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Endocrinopathy; Steroid; Pancreatic hormone; Adipose tissue; Estrogen; Cardiovascular disease; Lipids; Hydrocortisone; Metabolic syndrome; Glucocorticoid; Adiponectin; Protein hormone; 11β-Hydroxysteroid dehydrogenase; Corticosteroid; Enzyme; Steroid hormone; Cytokine; Metabolic diseases; Inflammation; Metabolism; Insulin; cortisol; Leptin; Adrenal hormone; Oxidoreductases; Sex steroid hormone
• DOI: 10.2174/092986707782359972
• ISSN: 0929-8673

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 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) 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 11βHSD1 enzyme activity, attenuating it in liver, kidney, and testis but upregulating 11βHSD1 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.