Hormonal control of regional fat distribution.
Hormones exert powerful influences on body fat distribution in humans. Studies under fully controlled conditions in vitro have indicated that cortisol and insulin facilitate lipid accumulation by expressing lipoprotein lipase (LPL). Growth hormone (GH) abolishes this and turns metabolism towards lipid mobilization. Testosterone and GH inhibit LPL and stimulate lipolysis markedly. Cortisol effects are mediated via a glucocorticoid receptor, and testosterone effects via an androgen receptor, the density of which appears to be higher in visceral than subcutaneous adipose tissue. The receptor-mediated effects are probably expressed via transcription of appropriate genes. The female sex steroids also regulate adipose tissue metabolism, but apparently not directly in the absence of specific cellular receptors. Oestrogens seem to exert net effects similar to those of testosterone. These results of cellular studies agree well with in-vivo studies of triglyceride uptake and turnover in different adipose tissue regions. Furthermore, clinical entities with characteristic disturbances in hormone levels show the expected redistribution patterns.
Björntorp
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Department of Heart and Lung Diseases, Sahlgren's Hospital, University of Göteborg, Sweden.
D000273:Adipose Tissue / Q000378:metabolism*; D001824:Body Constitution / Q000502:physiology*; D004967:Estrogens / Q000378:metabolism; D005260:Female; D006728:Hormones / Q000378:metabolism*; D019382:Human Growth Hormone / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D008066:Lipolysis / Q000502:physiology*; D008297:Male; D011374:Progesterone / Q000378:metabolism; D013739:Testosterone / Q000378:metabolism
D004967:Estrogens; D006728:Hormones; D019382:Human Growth Hormone; D013739:Testosterone; D011374:Progesterone; D006854:Hydrocortisone