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Am J Physiol Regul Integr Comp Physiol (October 30, 2003). doi:10.1152/ajpregu.00563.2003
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Submitted on September 26, 2003
Accepted on October 27, 2003

p38 Gamma MAPK Regulation of Glucose Transporter Expression and Glucose Uptake in L6 Myotubes and Mouse Skeletal Muscle

Richard C Ho1, Oscar Alcazar1, Nobuharu Fujii1, Michael F Hirshman1, and Laurie J Goodyear1*

1 Department of Medicine, Harvard Medical School, The Research Division, Joslin Diabetes Center, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: laurie.goodyear{at}joslin.harvard.edu.

Skeletal muscle expresses at least three p38 MAPKs ({alpha},{beta},{gamma}). However, no studies have examined the potential regulation of glucose uptake by p38{gamma}, the isoform predominantly expressed in skeletal muscle and highly regulated by exercise. L6 myotubes were transfected with empty vector (pCAGGS), activating MKK6 (MKK6CA), or p38{gamma}-specific siRNA. MKK6CA-transfected cells had higher rates of basal 3H-2-deoxyglucose (2DG) uptake (p<0.05), but lower rates of 2,4-dinitrophenol (DNP)-stimulated glucose uptake, an uncoupler of oxidative phosphoryaltion that operates through an insulin-independent mechanism (p<0.05). These effects were reversed when MKK6CA cells were cotransfected with p38{gamma}-specific siRNA. To determine whether the p38{gamma} isoform is involved in the regulation of contraction-stimulated glucose uptake in adult skeletal muscle, the tibialis anterior muscles of mice were injected with pCAGGS or wild-type p38{gamma} (p38{gamma}WT) followed by intramuscular electroporation. Basal and contraction-stimulated 2DG uptake in vivo was determined 14 days later. Overexpression of p38{gamma}WT resulted in higher basal rates of glucose uptake compared with pCAGGS (p<0.05). Muscles overexpressing p38{gamma}WT showed a trend for lower in situ contraction-mediated glucose uptake (P=0.08) and significantly lower total GLUT4 levels (p<0.05). These data suggest that p38{gamma} increases basal glucose uptake and decreases DNP- and contraction-stimulated glucose uptake, partially by affecting levels of glucose transporter expression in skeletal muscle. These findings are consistent with the hypothesis that activation of stress kinases such as p38 are negative regulators of stimulated glucose uptake in peripheral tissues.




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