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Lack of association between Glucocorticoid Receptor and 11beta‐HSD1 expression and muscle function in healthy older men and women
Author(s) -
Gallagher Iain,
Hyde Phillipa,
Stephens Nathan,
Gray Calum,
Ross James,
Fearon Kenneth,
Chapman Karen,
Greig Carolyn
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1049.6
Subject(s) - glucocorticoid receptor , glucocorticoid , medicine , endocrinology , sarcopenia , receptor , cortisone , 11β hydroxysteroid dehydrogenase type 1 , gene expression , chemistry , dehydrogenase , enzyme , gene , biochemistry
Increased glucocorticoid action may contribute to sarcopenia. We hypothesised that increased expression of the glucocorticoid amplifying enzyme, 11β‐hydroxysteroid dehydrogenase type 1 (11β‐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, cm 2 .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 11β‐HSD1 and NR3C1 was performed using real‐time PCR; data were analysed by t‐tests and correlation (R version 2.10). No differences in 11β‐HSD1 or NR3C1 mRNA were observed between sexes, nor were there significant associations between 11β‐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