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This Article Full Text Full Text (PDF) All Versions of this Article: 292/5/E1426    most recent 00524.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Burt, M. G. Articles by Ho, K. K. Y. Search for Related Content PubMed PubMed Citation Articles by Burt, M. G. Articles by Ho, K. K. Y.

Protein metabolism in glucocorticoid excess: study in Cushing's syndrome and the effect of treatment

¹Pituitary Research Unit, Garvan Institute of Medical Research; ²Department of Endocrinology, St. Vincent's Hospital; and ³University of New South Wales, Sydney, New South Wales, Australia

Submitted 26 September 2006 ; accepted in final form 19 January 2007

How protein metabolism is perturbed during chronic glucocorticoid excess is poorly understood. The aims were to investigate the impact of chronic glucocorticoid excess and restoration of eucortisolemia in Cushing's syndrome (CS) on whole body protein metabolism. Eighteen subjects with CS and 18 normal subjects (NS) underwent assessment of body composition using DEXA and whole body protein turnover with a 3-h constant infusion of L-[¹³C]leucine, allowing calculation of rates of leucine appearance (leucine R_a), leucine oxidation (L_ox), and leucine incorporation into protein (LIP). Ten subjects with CS were restudied after restoration of eucortisolemia. Percentage FM was greater (43.9 ± 1.6 vs. 33.8 ± 2.4%, P = 0.002) and LBM lower (52.7 ± 1.6 vs. 62.1 ± 2.3%, P = 0.002) in CS. LBM was significantly correlated (r² > 0.44, P < 0.005) to leuceine R_a, L_ox, and LIP in both groups. After correcting for LBM, leucine R_a (133 ± 5 vs. 116 ± 5 µmol/min, P = 0.02) and L_ox (29 ± 1 vs. 24 ± 1 µmol/min, P = 0.01) were greater in CS. FM significantly correlated (r² = 0.23, P < 0.05) with leucine R_a and LIP, but not L_ox in CS. In multiple regression, LBM was an independent determinant of all three indexes of leucine turnover, FM of leucine R_a, and LIP and CS of L_ox. Following restoration of eucortisolemia, L_ox was reduced (–7.5 ± 2.6 µmol/min, P = 0.02) and LIP increased (+15.2 ± 6.2 µmol/min, P = 0.04). In summary, whole body protein metabolism in CS is influenced by changes in body composition and glucocorticoid excess per se, which increases protein oxidation. Enhanced protein oxidation is a likely explanation for the reduced protein mass in CS. Successful treatment of CS reduces protein oxidation and increases protein synthesis to prevent ongoing protein loss.

whole body leucine turnover; body composition; resting energy expenditure

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