Aberrant p38 mitogen-activated protein kinase signalling in skeletal muscle from Type 2 diabetic patients
p38 mitogen activated protein kinase (MAPK) is generally thought to facilitate signal transduction to genomic, rather than metabolic responses. However, recent evidence implicates a role for p38 MAPK in the regulation of glucose transport; a site of insulin resistance in Type 2 diabetes. Thus we determined p38 MAPK protein expression and phosphorylation in skeletal muscle from Type 2 diabetic patients and non-diabetic subjects.
p38 MAPK protein expression was similar between Type 2 diabetic patients and non-diabetic subjects. Insulin exposure increased p38 MAPK phosphorylation in non-diabetic, but not in Type 2 diabetic patients. In contrast, basal phosphorylation of p38 MAPK was increased in skeletal muscle from Type 2 diabetic patients.
Insulin increases p38 MAPK phosphorylation in skeletal muscle from non-diabetic subjects, but not in Type 2 diabetic patients. However, basal p38 MAPK phosphorylation is increased in skeletal muscle from Type 2 diabetic patients. Thus, aberrant p38 MAPK signalling might contribute to the pathogenesis of insulin resistance.
- Aberrant p38 mitogen-activated protein kinase signalling in skeletal muscle from Type 2 diabetic patients
Volume 46, Issue 10 , pp 1324-1328
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- 5-AMP activated protein kinase
- 5-aminoimidazole-4-carboxamide ribonucleoside
- insulin signalling
- glucose transport
- mitogen-activated protein kinase
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- Author Affiliations
- 1. Department of Surgical Sciences, Section for Integrative Physiology, Karolinska Institutet, von Eulers väg 4, II tr, 171 77, Stockholm, Sweden
- 2. Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland
- 3. Biomedicum, Helsinki, Finland