Acute Hypercortisolemia Exerts Depot-Specific Effects on Abdominal and Femoral Adipose Tissue Function.
BACKGROUND
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.


METHODS
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.
Institute of Metabolism and Systems Research, University of Birmingham B15 2TT, United Kingdom.|Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham B15 2TH, United Kingdom.
Konstantinos N
KN
Manolopoulos
Institute of Metabolism and Systems Research, University of Birmingham B15 2TT, United Kingdom.|Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham B15 2TH, United Kingdom.
Michael W
MW
O'Reilly
Institute of Metabolism and Systems Research, University of Birmingham B15 2TT, United Kingdom.
Iwona J
IJ
Bujalska
Oxford Centre for Diabetes, Endocrinology and Metabolism, National Institute for Health Research Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, United Kingdom.
Jeremy W
JW
Tomlinson
Institute of Metabolism and Systems Research, University of Birmingham B15 2TT, United Kingdom.|Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham B15 2TH, United Kingdom.|National Institute for Health Research Birmingham Liver Biomedical Research Unit, University Hospitals Birmingham, National Health Service Foundation Trust, Birmingham B15 2TH, United Kingdom.
Wiebke
W
Arlt
D000005:Abdomen; D015502:Absorptiometry, Photon; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000328:Adult; D003480:Cushing Syndrome / Q000139:chemically induced* / Q000378:metabolism; D004311:Double-Blind Method; D005269:Femur; D006801:Humans; D006854:Hydrocortisone / Q000008:administration & dosage* / Q000097:blood; D008066:Lipolysis / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D050507:Subcutaneous Fat, Abdominal / Q000187:drug effects* / Q000378:metabolism; D013848:Thigh; D055815:Young Adult
D006854:Hydrocortisone