Lack of association between Glucocorticoid Receptor and 11beta-HSD1 expression and muscle function in healthy older men and women

Iain Gallagher, Phillipa Hyde, Nathan Stephens, Calum Gray, James Ross, Kenneth Fearon, Karen Chapman, Carolyn Greig

Research output: Contribution to journalMeeting abstractpeer-review

Abstract

Increased glucocorticoid action may contribute to sarcopenia. We hypothesised that increased expression of the glucocorticoid amplifying enzyme, 11$-hydroxysteroid dehydrogenase type 1 (11$-HSD1, which converts intrinsically inert cortisone to active cortisol) and the glucocorticoid receptor (encoded by NR3C1) would be negatively associated with muscle function and systemic inflammation (C-reactive protein; CRP) in healthy older human muscle. We recruited n=16 men (79.0 ± 3.6y) and n=14 women (79.3 ± 3.4y). We measured quadriceps cross-sectional area (CSA, cm2.m–2), isometric knee extensor strength (IKES, N.kg–1) and lower limb power (LLEP, W.kg–1) and sampled venous blood for CRP. Muscle samples were obtained from the lateral quadriceps. Relative quantification of mRNA for 11$-HSD1 and NR3C1 was performed using real-time PCR; data were analysed by t-tests and correlation (R version 2.10). No differences in 11$-HSD1 or NR3C1 mRNA were observed between sexes, nor were there significant associations between 11$-HSD1 or NR3C1 and muscle CSA (r= –0.6, p=0.8; r= 0.32, p=0.17), IKES (r= –0.37, p=0.08; r= –0.22, p=0.32), LLEP (r= –0.17, p=0.44; r= 0.00, p=0.1) and CRP (r= –0.13, p=0.56; r= 0.25, p=0.24) respectively. These preliminary data suggest that regulation of glucocorticoid activity via the action of these genes may not be a major contributor to human sarcopenia. Supported by UK Physiological Society
Original languageUndefined/Unknown
Pages (from-to)1049.6
JournalThe FASEB Journal
Volume25
Issue number1MeetingAbstracts
Publication statusPublished - 1 Mar 2011

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