Journal
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
Volume 111, Issue 7, Pages 1553-1558Publisher
SPRINGER
DOI: 10.1007/s00421-010-1783-1
Keywords
ER stress; High-fat diet; Lipotoxicity; BiP; Intramyocellular lipids
Categories
Funding
- Fonds National de la Recherche Scientifique (Belgium)
- Fonds de la Recherche Scientifique Medicale (FRSM) [3.4514.]
- Universite catholique de Louvain
- Katholieke Universiteit Leuven [OT/05/53]
- Fund for Scientific Research-Flanders, Belgium (F.W.O.-Vlaanderen) [G.0233.05 F]
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Endoplasmic reticulum (ER) stress in pancreas, liver, and adipose tissue is a key event in the pathogenesis of obesity-related metabolic disease. Lipid-induced ER stress in liver and adipose tissue leads to inhibition of insulin signaling. Whether this mechanism exists in skeletal muscle is currently unknown. The present study aimed at assessing the ER stress response in skeletal muscle of subjects receiving a hyper-caloric fat-rich diet (HFD). Seven healthy males (20.6 +/- A 0.5 years; 70.9 +/- A 3.4 kg) volunteered to participate in the study. They received a hyper-caloric (+30% kcal) fat-rich (50% kcal) diet for 6 weeks. An oral glucose tolerance test (OGTT) was performed, and muscle biopsies were taken before and after HFD. HFD increased body mass by similar to 3 kg (P = 0.007) and the sum of skinfolds by 15% (P = 0.003). After HFD, blood glucose concentrations were higher during OGTT (two-way ANOVA, P = 0.023; +45% at 20 min, P = 0.002), and fasting plasma insulin level tended to be higher (+20%). HFD increased intramyocellular lipids content by similar to 50 and 75% in type I (P = 0.0009) and IIa fibers (P = 0.002), respectively. The protein expression of inositol-requiring enzyme 1 alpha, protein kinase R-like ER protein kinase, BiP and calnexin and the mRNA level of spliced X box binding protein-1, CCAAT/enhancer binding protein homologous protein and activating transcription factor 4 were not changed after HFD. Despite the increase in body mass, subcutaneous fat deposits, and intramyocellular lipids content, ER stress markers were unchanged in skeletal muscle of subjects receiving a HFD for 6 weeks. This suggests that the onset of glucose intolerance is not related to ER stress in skeletal muscle.
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