Knockdown of NYGGF4 increases glucose transport in C2C12 mice skeletal myocytes by activation IRS-1/PI3K/AKT insulin pathway

NYGGF4, an obesity-related gene, is proposed to be involved in the development of insulin resistance. Skeletal muscle is a primary target organ for insulin and NYGGF4 showed a relatively high expression level in skeletal muscle. Therefore, this study aimed to explore the effect of NYGGF4 on insulin...

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Bibliographic Details
Published in:Journal of bioenergetics and biomembranes 2012-06, Vol.44 (3), p.351-355
Main Authors: Zeng, Xue-Qi, Zhang, Chun-Mei, Tong, Mei-Ling, Chi, Xia, Li, Xi-Ling, Ji, Chen-Bo, Zhang, Rong, Guo, Xi-Rong
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Animal Anatomy
Animal Biochemistry
Animals
Biochemistry
Bioorganic Chemistry
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cell Culture Techniques
Cell Differentiation - physiology
Chemistry
Chemistry and Materials Science
Data processing
Gene Knockdown Techniques
Glucose
Glucose - metabolism
Glucose transport
Histology
Insulin
Insulin - metabolism
Insulin receptor substrate 1
Insulin Receptor Substrate Proteins - metabolism
Mice
Morphology
Muscle Fibers, Skeletal - cytology
Muscle Fibers, Skeletal - metabolism
Myoblasts - metabolism
Myocytes
Organic Chemistry
Phosphatidylinositol 3-Kinases - metabolism
Phosphorylation
Proto-Oncogene Proteins c-akt - metabolism
RNA-mediated interference
Rodents
Signal Transduction
Skeletal muscle
Skeletal system
Transfection
Translocation
Western blotting
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Summary:NYGGF4, an obesity-related gene, is proposed to be involved in the development of insulin resistance. Skeletal muscle is a primary target organ for insulin and NYGGF4 showed a relatively high expression level in skeletal muscle. Therefore, this study aimed to explore the effect of NYGGF4 on insulin sensitivity of skeletal muscle cells. RNA interference (RNAi) was adopted to silence NYGGF4 expression in mice C2C12 skeletal myocytes. A remarkably increased insulin-stimulated glucose uptake and GLUT4 translocation was observed in NYGGF4 silencing C2C12 cells. Importantly, the enhanced glucose uptake induced by NYGGF4 silencing could be abrogated by the PI3K inhibitor LY294002. In addition, the crucial molecules involved in PI3K insulin signaling pathway were detected by western blotting. The results showed that NYGGF4 knockdown dramatically activate the insulin-stimulated phosphorylation of IRS-1 and AKT. Taken together, these data demonstrate that NYGGF4 knockdown increases glucose transport in myocytes by activation of the IRS-1/PI3K/AKT insulin pathway.
ISSN:0145-479X
1573-6881
DOI:10.1007/s10863-012-9438-z