Over-expression of NYGGF4 (PID1) inhibits glucose transport in skeletal myotubes by blocking the IRS1/PI3K/AKT insulin pathway

Wu, Weiling; Gan, Weihua; Tong, Meiling; Li, X.L.; DAI, JIARONG; Zhang, C.M.; Guo, Xirong

doi:10.1016/j.ymgme.2010.11.165

Cited by 44 publications

(32 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One of these genes, Cblb, encodes a ubiquitin E3 ligase involved in IRS-1 degradation (18). Pid-1 inhibits the tyrosine phosphorylation of IRS-1 (19). Grb10 inhibits the physical interaction between IR and IRS-1 (20).…”

Section: Resultsmentioning

confidence: 99%

Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling

Kuo¹,

Lew²,

Mayba

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

129

127

View full text Add to dashboard Cite

Glucocorticoids elicit a variety of biological responses in skeletal muscle, including inhibiting protein synthesis and insulin-stimulated glucose uptake and promoting proteolysis. Thus, excess or chronic glucocorticoid exposure leads to muscle atrophy and insulin resistance. Glucocorticoids propagate their signal mainly through glucocorticoid receptors (GR), which, upon binding to ligands, translocate to the nucleus and bind to genomic glucocorticoid response elements to regulate the transcription of nearby genes. Using a combination of chromatin immunoprecipitation sequencing and microarray analysis, we identified 173 genes in mouse C2C12 myotubes. The mouse genome contains GR-binding regions in or near these genes, and gene expression is regulated by glucocorticoids. Eight of these genes encode proteins known to regulate distinct signaling events in insulin/insulin-like growth factor 1 pathways. We found that overexpression of p85α, one of these eight genes, caused a decrease in C2C12 myotube diameters, mimicking the effect of glucocorticoids. Moreover, reducing p85α expression by RNA interference in C2C12 myotubes significantly compromised the ability of glucocorticoids to inhibit Akt and p70 S6 kinase activity and reduced glucocorticoid induction of insulin receptor substrate 1 phosphorylation at serine 307. This phosphorylation is associated with insulin resistance. Furthermore, decreasing p85α expression abolished glucocorticoid inhibition of protein synthesis and compromised glucocorticoid-induced reduction of cell diameters in C2C12 myotubes. Finally, a glucocorticoid response element was identified in the p85α GR-binding regions. In summary, our studies identified GR-regulated transcriptional networks in myotubes and showed that p85α plays a critical role in glucocorticoidinduced insulin resistance and muscle atrophy in C2C12 myotubes.

show abstract

Section: Resultsmentioning

confidence: 99%

Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling

Kuo¹,

Lew²,

Mayba

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

129

127

View full text Add to dashboard Cite

show abstract

“…Until now, research topics focus on the PID1 gene cloning, the relationship between PID1 and insulin resistance, and the underlying mechanism and signal pathways of its role in insulin resistance (Zhang et al 2009;Zhao et al 2010a,b;Man et al 2011;Wu et al 2011;Chen et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Porcine phosphotyrosine interaction domain containing 1 modulates 3T3-L1 preadipocyte proliferation and differentiation

et al. 2013

View full text Add to dashboard Cite

Abstract:The phosphotyrosine interaction domain containing 1 (PID1) gene was firstly isolated from obese subjects and involved in obesity-associated insulin resistance. In the present study, Duroc×Landrace×Yorkshire (DLY) pig PID1 cDNA was cloned. The entire open reading frame of the cloned porcine PID1 is 654 bp. The predicted protein is composed of 217 amino acids residues with a molecular mass of 24,774 Da. Over-expression of porcine PID1 significantly accelerated the proliferation of 3T3-L1 preadipocyte, but inhibited preadipocyte differentiation by decreasing the numerous fat droplets appeared and down-regulating the mRNA expression levels of peroxisome proliferators-activated receptor-γ, CCAAT/enhancer binding protein α, fat acid synthase and lipoprotein lipase. Together, these results suggest that porcine PID1 plays a role in regulating adipose development.

show abstract

“…The overexpression of NYGGF4 has been shown to inhibit insulinstimulated glucose transport and impair GLUT4 translocation in mature adipocytes by blocking signals in the classical insulin-signaling pathway (Wu et al, 2011). Consistent with this, Wang et al (2012) showed that overexpressing the gene NYGGF4 in adipocytes, led to significantly increased levels of ROS and inhibition of glucose uptake into adipocytes.…”

Section: Oxidative Stress and Insulin Resistancementioning

confidence: 67%

Effects of Postmeal Walking on Postprandial Glucose Control and Oxidative Stress

Knurick

Johnston

2016

Medicine & Science in Sports & Exercise

View full text Add to dashboard Cite

Background: Postprandial hyperglycemia can increase levels of oxidative stress and is an independent risk factor for complications associated with type 2 diabetes. Purpose:To evaluate the acute effects of a 15-min postmeal walk on glucose control and markers of oxidative stress following a high-carbohydrate meal.Methods: Ten obese subjects (55.0 ± 10.0 yrs) with impaired fasting glucose (107.1 ± 9.0 mg/dL) participated in this repeated measures trial. Subjects arrived at the laboratory following an overnight fast and underwent one of three conditions: 1) Test meal with no walking or fiber (CON), 2) Test meal with 10g fiber and no walking (FIB), 3) Test meal with no fiber followed by a 15-min treadmill walk at preferred walking speed (WALK).Blood samples were taken over four hours and assayed for glucose, insulin, thiobarbituric reactive substances (TBARS), catalase, uric acid, and total antioxidant capacity (TAC). A iii ACKNOWLEDGEMENTS

show abstract

Over-expression of NYGGF4 (PID1) inhibits glucose transport in skeletal myotubes by blocking the IRS1/PI3K/AKT insulin pathway

Cited by 44 publications

References 19 publications

Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling

Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling

Porcine phosphotyrosine interaction domain containing 1 modulates 3T3-L1 preadipocyte proliferation and differentiation

Effects of Postmeal Walking on Postprandial Glucose Control and Oxidative Stress

Contact Info

Product

Resources

About