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Regulation of insulin response in skeletal muscle cell by caveolin status
Author(s) -
Oh Yoon Sin,
Cho Kyung A.,
Ryu Sung Jin,
Khil LeeYong,
Jun HeeSook,
Yoon JiWon,
Park Sang Chul
Publication year - 2006
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20943
Subject(s) - caveolae , caveolin 1 , caveolin 3 , caveolin , downregulation and upregulation , skeletal muscle , myocyte , insulin receptor , microbiology and biotechnology , medicine , endocrinology , biology , protein kinase b , insulin , phosphorylation , colocalization , chemistry , signal transduction , insulin resistance , biochemistry , gene
Recent studies on the role of caveolin‐1 in adipocytes showed that caveolin has emerged as an important regulatory element in insulin signaling but little is known on its role in skeletal muscle cells. In this study, we demonstrate for the first time that caveolin‐1 plays a crucial role in insulin dependent glucose uptake in skeletal muscle cells. Differentiation of L6 skeletal muscle cells induce the expression of caveolin‐1 and caveolin‐3 with partial colocalization. However in contrast to adipocytes, phosphorylation of insulin receptor β (IRβ) and Akt/Erk was not affected by the respective downregulation of caveolin‐1 or caveolin‐3 in the muscle cells. Moreover, the phosphorylation of IRβ was detected not only in the caveolae but also in the non‐caveolae fractions of the muscle cells despite the interaction of IRβ with caveolin‐1 and caveolin‐3. These data implicate the lack of relationship between caveolins and IRβ pathway in the muscle cells, different from the adipocytes. However, glucose uptake was reduced specifically by downregulation of caveolin‐1, but not that of caveolin‐3. Taken together, these observations suggest that caveolin‐1 plays a crucial role in glucose uptake in differentiated muscle cells and that the regulation of caveolin‐1 expression may be an important mechanism for insulin sensitivity, implying the role of muscle cells for type 2 diabetes. J. Cell. Biochem. 99: 747–758, 2006. © 2006 Wiley‐Liss, Inc.