## Abstract Major problems in stem cell biology revolve around defining the developmental potential of cell populations and understanding how their potential is maintained or progressively restricted. Oxygen (O~2~) is an obvious environmental factor which has received little attention in culturing
Regulation of insulin response in skeletal muscle cell by caveolin status
✍ Scribed by Yoon Sin Oh; Kyung A. Cho; Sung Jin Ryu; Lee-Yong Khil; Hee-Sook Jun; Ji-Won Yoon; Sang Chul Park
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 482 KB
- Volume
- 99
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
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.
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