Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism
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 depo...
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Published in | Current medicinal chemistry Vol. 14; no. 27; pp. 2918 - 2924 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Schiphol
Bentham Science Publishers Ltd
01.11.2007
Bentham Science |
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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 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. |
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AbstractList | 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. 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. |
Author | Cecilia Mattsson Tommy Olsson |
Author_xml | – sequence: 1 givenname: Cecilia surname: MATTSSON fullname: MATTSSON, Cecilia organization: Department of Medicine and Public Health, UmeÅ University Hospital, UmeÅ, Sweden – sequence: 2 givenname: Tommy surname: OLSSON fullname: OLSSON, Tommy organization: Department of Medicine and Public Health, UmeÅ University Hospital, UmeÅ, Sweden |
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Keywords | 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 |
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SubjectTerms | 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 |
Title | Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism |
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