Altering dietary nutrient intake that reduces glycogen content leads to phosphorylation of nuclear p38 MAP kinase in human skeletal muscle: association with IL‐6 gene transcription during contraction

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Abstract
To determine the effect of glycogen availability and contraction on intracellular signaling and IL‐6 gene transcription, eight males performed 60 min of exercise on two occasions: either with prior ingestion of a normal (Con) or low carbohydrate (LCHO) diet that reduced pre‐exercise muscle glycogen content. Muscle biopsies were obtained and analyzed for IL‐6 mRNA. In addition, nuclear proteins were isolated from the samples and analyzed for the mitogen‐ activated protein kinases (MAPK) c‐jun amino‐terminal kinase (JNK) 1 and 2 and p38 MAPK. Nuclear fractions were also analyzed for the phosphorylated forms of JNK (p‐JNK) and p38 MAPK (p‐ p38 MAPK) and the abundance of the nuclear transcription factors nuclear factor of activated T cells (NFAT) and nuclear factor kappa‐β (NF‐κβ). No differences were observed in the protein abundance of total JNK 1/2, p38 MAPK, NFAT, or NF‐κβ before exercise, but the nuclear abundance of p‐p38 MAPK was higher (PPPr=0.96; PPPP<0.05) the ionomycin‐ induced increase in IL‐6 mRNA. These data suggest that reduced carbohydrate intake that results in low intramuscular glycogen leads to phosphorylation of p38 MAPK at the nucleus. Furthermore, phosphorylation of p38 MAPK in the nucleus appears to be an upstream target for IL‐6, providing new insights into the regulation of IL‐6 gene transcription.
Funding Information
  • National Health and Medical Research Council

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