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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 2 626-631
Copyright © 1998 by The Endocrine Society

Original Studies

Effects of Physiological Hypercortisolemia on the Regulation of Lipolysis in Subcutaneous Adipose Tissue1

Jaswinder S. Samra, Mo L. Clark, Sandy M. Humphreys, Ian A. MacDonald, Peter A. Bannister and Keith N. Frayn

Oxford Lipid Metabolism Group, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Oxford, United Kingdom OX2 6HE; the Department of Physiology and Pharmacology, Medical School, Queen’s Medical Center (I.A.M.), Nottingham, United Kingdom NG7 2UH; and the Unit of Metabolic Medicine, Imperial College School of Medicine at St. Mary’s (P.A.B.), London, United Kingdom W2 1PG

Address all correspondence and requests for reprints to: Dr. Keith N. Frayn, Oxford Lipid Metabolism Group, Radcliffe Infirmary, Oxford, OX2 6HE United Kingdom. E-mail: keith.frayn{at}oxlip.ox.ac.uk

Cortisol is known to increase whole body lipolysis, yet chronic hypercortisolemia results in increased fat mass. The main aim of the study was to explain these two apparently opposed observations by examining the acute effects of hypercortisolemia on lipolysis in subcutaneous adipose tissue and in the whole body. Six healthy subjects were studied on two occasions. On one occasion hydrocortisone sodium succinate was infused iv to induce hypercortisolemia (mean plasma cortisol concentrations, 1500 ± 100 vs. 335 ± 25 nmol/L; P < 0.001); on the other occasion (control study) no intervention was made.

Lipolysis in the sc adipose tissue of the anterior abdominal wall was studied by measurement of arterio-venous differences, and lipolysis in the whole body was studied by constant infusion of [1,2,3-2H5]glycerol for measurement of the systemic glycerol appearance rate. Hypercortisolemia led to significantly increased arterialized plasma nonesterified fatty acid (NEFA; P < 0.01) and blood glycerol concentrations (P < 0.05), with an increase in systemic glycerol appearance (P < 0.05). However, in sc abdominal adipose tissue, hypercortisolemia decreased veno-arterialized differences for NEFA (P < 0.05) and reduced NEFA efflux (P < 0.05). This reduction was attributable to decreased intracellular lipolysis (P < 0.05), reflecting decreased hormone-sensitive lipase action in this adipose depot. Hypercortisolemia caused a reduction in arterialized plasma TAG concentrations (P < 0.05), but without a significant change in the local extraction of TAG (presumed to reflect the action of adipose tissue lipoprotein lipase). There was no significant difference in plasma insulin concentrations between the control and hypercortisolemia study. Site-specific regulation of the enzymes of intracellular lipolysis (hormone-sensitive lipase) and intravascular lipolysis (lipoprotein lipase) may explain the ability of acute cortisol treatment to increase systemic glycerol and NEFA appearance rates while chronically promoting net central fat deposition.




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