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1 Noll Physiological Research Center and Departments of 2 Biobehavioral Health and Clinical Medicine, 3 Veterinary Science, and 4 Molecular and Cellular Physiology, The Pennsylvania State University, University Park, Pennsylvania 16802; and 5 Department of Clinical Physiology, Karolinska Hospital, Karolinska Institute, SE 171-76, Stockholm, Sweden
Physiological stress
associated with muscle damage results in systemic insulin resistance.
However, the mechanisms responsible for the insulin resistance are not
known; therefore, the present study was conducted to elucidate the
molecular mechanisms associated with insulin resistance after muscle
damage. Muscle biopsies were obtained before (base) and at 1 h
during a hyperinsulinemic-euglycemic clamp (40 mU · kg
1 · min1) in eight young (age
24 ± 1 yr) healthy sedentary (maximal O2 consumption,
49.7 ± 2.4 ml · kg1 · min1) males before and 24 h after eccentric exercise
(ECC)-induced muscle damage. To determine the role of cytokines in
ECC-induced insulin resistance, venous blood samples were obtained
before (control) and 24 h after ECC to evaluate ex vivo
endotoxin-induced mononuclear cell secretion of tumor necrosis factor
(TNF)-
, interleukin (IL)-6, and IL-1
. Glucose disposal was 19%
lower after ECC (P < 0.05). Insulin-stimulated insulin
receptor substrate (IRS)-1 tyrosine phosphorylation was 45% lower
after ECC (P < 0.05). Insulin-stimulated phosphatidylinositol (PI) 3-kinase, Akt (protein kinase B) serine phosphorylation, and Akt activity were reduced 34, 65, and 20%, respectively, after ECC (P < 0.05). TNF-, but not
IL-6 or IL-1 production, increased 2.4-fold 24 h after ECC
(P < 0.05). TNF- production was positively
correlated with reduced insulin action on PI 3-kinase
(r = 0.77, P = 0.04). In summary, the
physiological stress associated with muscle damage impairs insulin
stimulation of IRS-1, PI 3-kinase, and Akt-kinase, presumably leading
to decreased insulin-mediated glucose uptake. Although more research is
needed on the potential role for TNF- inhibition of insulin action, elevated TNF- production after muscle damage may impair insulin signal transduction.
tumor necrosis factor-; cytokines; signal transduction; stress
diabetes; glucose uptake
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