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Exercise Training Protects Against Overexposure to Glucocorticoids in Skeletal Muscle and Liver Tissue in the Fructose‐Fed Hamster
Author(s) -
Campbell Jonathan Edward,
Fediuc Sergiu,
Hawke Thomas James,
Riddell Michael Charles
Publication year - 2006
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.20.4.a300-a
Subject(s) - medicine , endocrinology , skeletal muscle , insulin resistance , fructose , chemistry , hamster , insulin , biochemistry
Elevated exposure to glucocorticoids (GC) in insulin target tissues has been linked to insulin resistance. Tissue exposure to GC is determined by both the receptor (GR) and the pre‐receptor enzyme, 11beta‐hydroxysteroid dehydrogenase type 1(11βHSD1), which converts inactive GC to the active form. We tested the hypothesis that beneficial effects of exercise are mediated through changes in the expression of 11βHSD1 and GR in skeletal muscle and liver. Male Syrian hamsters were divided into 3 groups; fructose‐fed exercise (FE), fructose‐fed sedentary (FS), and chow‐fed sedentary (CS). FE had access to running wheels for 6 wks and all were sacrificed following an intraperitoneal glucose tolerance test (IPGTT). Combining the AUC for glucose and insulin yields an insulin sensitivity index, which indicated that FS was significantly more insulin resistant than either CS or FE (p<0.05). Gastrocnemius 11βHSD1 protein level was lower in FE (0.66 0.12 relative optical density [ROD]) compared to CS (1.00 0.05 ROD) or FS (0.92±0.06 ROD, p<0.05), while GR was similar between groups. Liver GR was lower in FE (0.66±0.09 ROD) compared to both CS (1.00±0.08 ROD) and FS (0.95±0.09 ROD, p<0.05), while 11βHSD1 was similar between groups. Thus, exercise decreases the determinants of tissue GC exposure in muscle and liver and is associated with retention in insulin sensitivity despite a high‐fructose diet.