4.2 Article

Sex- and Depot-specific Lipolysis Regulation in Human Adipocytes: Interplay between Adrenergic Stimulation and Glucocorticoids

Journal

HORMONE AND METABOLIC RESEARCH
Volume 40, Issue 12, Pages 854-860

Publisher

GEORG THIEME VERLAG KG
DOI: 10.1055/s-0028-1087168

Keywords

visceral; subcutaneous; adipose tissue; cAMP; dexamethasone

Funding

  1. Swedish Research Council [14287]
  2. Swedish Diabetes Association
  3. Faculty of Medicine at Umea University
  4. AstraZeneca RD
  5. Novo Nordisk
  6. Sigurd and Elsa Golje
  7. Torsten and Ragnar Soderberg foundations

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The purpose of this investigation was to explore interactions between adrenergic Stimulation, glucocorticoids, and insulin on the lipolytic rate in isolated human adipocytes from subcutaneous and omental fat depots, and to address possible sex differences. Fat biopsies were obtained from 48 nondiabetic subjects undergoing elective abdominal Surgery. Lipolysis rate was measured as glycerol release from isolated cells and proteins involved in lipolysis regulation were assessed by immunoblots. Fasting blood samples were obtained and metabolic and inflammatory, variables were analyzed. In women, the rate of 8-bromo-cAMP- and isoprenaline-stimulated lipolysis was similar to 2- and 1.5-fold higher, respectively, in subcutaneous compared to omental adipocytes, whereas there was no difference between the two depots in men. Dexamethasone treatment increased the ability of 8-bromo-cAMP to stimulate lipolysis in the subcutaneous depot in women, but had no consistent effects in fat cells from men. Protein kinase A, Perilipin A, and hormone sensitive lipase content in adipocytes was not affected by adipose depot, sex, or glucocorticoid treatment. In conclusion, catecholamine and glucocorticoid regulation of lipolysis in isolated human adipocytes differs between adipose tissue depots and also between sexes. These findings may be of relevance for the interaction between endogenous stress hormones and adipose tissue function in visceral adiposity and the metabolic syndrome.

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