Acute hypercortisolemia exerts depot-specific effects on abdominal and femoral adipose tissue function

Research output: Contribution to journalArticle

Colleges, School and Institutes

External organisations

  • Oxford Centre for Diabetes, Endocrinology and Metabolism, and NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, UK

Abstract

Context:
Glucocorticoids have pleiotropic metabolic functions, and acute glucocorticoid excess affects fatty acid metabolism, increasing systemic lipolysis. Whether glucocorticoids exert adipose tissue depot-specific effects remains unclear.
Objective:
To provide an in vivo assessment of femoral and abdominal adipose tissue responses to acute glucocorticoid administration.
Design and Outcome Measures:
Nine healthy male volunteers were studied on two occasions, after a hydrocortisone infusion (0.2 mg/kg/min for 14 hours) and a saline infusion, respectively, given in randomized double-blind order. The subjects were studied in the fasting state and after a 75-g glucose drink with an in vivo assessment of femoral adipose tissue blood flow (ATBF) using radioactive xenon washout and of lipolysis and glucose uptake using the arteriovenous difference technique. In a separate study (same infusion design), eight additional healthy male subjects underwent assessment of fasting abdominal ATBF and lipolysis only. Lipolysis was assessed as the net release of nonesterified fatty acids (NEFAs) from femoral and abdominal subcutaneous adipose tissue.
Results:
Acute hypercortisolemia significantly increased basal and postprandial ATBF in femoral adipose tissue, but the femoral net NEFA release did not change. In abdominal adipose tissue, hypercortisolemia induced substantial increases in basal ATBF and NEFA release.
Conclusions:
Acute hypercortisolemia induces differential lipolysis and ATBF responses in abdominal and femoral adipose tissue, suggesting depot-specific glucocorticoid effects. Abdominal, but not femoral, adipose tissue contributes to the hypercortisolemia-induced systemic NEFA increase, with likely contributions from other adipose tissue sources and intravascular triglyceride hydrolysis.

Details

Original languageEnglish
Pages (from-to)1091-1101
JournalJournal of Clinical Endocrinology and Metabolism
Volume102
Issue number4
Early online date16 Feb 2017
Publication statusE-pub ahead of print - 16 Feb 2017