|
Hyperglycemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results suggest that enhancing IRS-1-dependent p53 stabilization could attenuate the progression of atherosclerotic lesions in hyperglycemia and insulin-resistance states.
|
30578299 |
2019 |
|
Hyperglycemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Collectively, these data indicate that PNS reduces hyperglycemia and insulin resistance through up-regulating GLUT4 expression and the IRS1-PI3K-AKT signaling pathway.
|
30945455 |
2019 |
|
Hyperglycemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Metformin blocked the inhibitory effect of insulin-like growth factor 1 receptor (IGF-1R)/insulin receptor substrate 1 (IRS-1) pathway on TSC-2, and hyperglycemia impaired metformin-induced inhibition of IGF-1R/IRS-1 pathway and modulated the invasiveness of bile duct cancer cells; however, this effect was impaired by hyperglycemia.
|
31205529 |
2019 |
|
Hyperglycemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Effect of Long-term Administration of Oral Magnesium Sulfate and Insulin to Reduce Streptozotocin-Induced Hyperglycemia in Rats: the Role of Akt2 and IRS1 Gene Expressions.
|
30519800 |
2019 |
|
Hyperglycemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
In vivo hyperglycemia/hyperinsulinemia in rats for 48 hours similarly resulted in activation of PKC-ζ and increased phosphorylation of IRS-1 Ser318 and Akt Thr34.
|
29370351 |
2018 |
|
Hyperglycemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Genetic reduction of p52Shc minimizes competition with IRS1, and improves insulin signaling and glucose control in mice, and improves pathophysiological consequences of hyperglycemia.
|
30290222 |
2018 |
|
Hyperglycemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Insulin receptor and insulin receptor substrate-1 (IRS-1) messenger RNA, known stimulate to membrane translocation of Gluts, were both decreased by the HG condition but not by the NG condition.
|
28624040 |
2017 |
|
Hyperglycemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here we show that deletion of IRS-1 expression in VSMCs in non-diabetic mice results in dedifferentiation, SHPS-1 activation, and aberrant signaling and that these changes parallel those that occur in response to hyperglycemia.
|
28003360 |
2017 |
|
Hyperglycemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The underlying mechanisms of these beneficial effects of ACH09 may involve the activation of hepatic insulin-signaling pathway because the expression of phosphorylated insulin receptor substrate-1, phosphatidylinositol 3-kinase, phosphorylated Akt serine/threonine kinase 1, and glucose transporter 2 was increased by ACH09 and correlated with improvement of hyperglycemia, hyperinsulinemia, and insulin resistance.
|
28739056 |
2017 |
|
Hyperglycemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Given their central role in the insulin signalling pathway, it is not surprising that male mice lacking Irs1 or Irs2 present with elevated blood glucose or type 2 diabetes, respectively.
|
27514532 |
2016 |
|
Hyperglycemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our data suggest that the degradation of IRS-1 by HCV core protein translates to impaired ability of insulin to inhibit the expression of the target gene IGFBP-1 in the liver and may serve as a novel mechanism for insulin resistance and hyperglycaemia.
|
22187946 |
2012 |
|
Hyperglycemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, diabetes-related hyperglycemia hyperactivates the mTOR pathway and may lead to insulin resistance due to suppression of IRS-1-dependent PI3-kinase/Akt signaling.
|
16354680 |
2006 |
|
Hyperglycemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Hyperglycemia (25 mM glucose) and TNF-alpha showed analogous (> 50% inhibition) effects on tyrosine phosphorylation of insulin receptor substrate-1, Shc, p60, and p44, whereas opposite effects were observed for tyrosine phosphorylation of FAK125, which is dephosphorylated after insulin stimulation.
|
8617880 |
1996 |