Hyperinsulinism
|
0.400 |
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 |
Hyperinsulinism
|
0.400 |
Biomarker
|
disease |
BEFREE |
In obesity and type 2 diabetes, selective downregulation of Irs2 and its downstream actions to cause reduced insulin actions was associated with increased insulin actions through Irs1 in variety tissues.
|
28380373 |
2017 |
Hyperinsulinism
|
0.400 |
Biomarker
|
disease |
BEFREE |
Additionally, TBF treatment significantly reduced phosphorylation of insulin receptor substrate 1 (IRS-1) at serine 307 and increased insulin-stimulated Akt/eNOS activation in the SHRs.
|
29043342 |
2017 |
Hyperinsulinism
|
0.400 |
Biomarker
|
disease |
BEFREE |
We characterised expression of IR-related molecules, IRS-1 phosphorylation and downstream signalling in a panel of 5 colon cancer cell lines at different insulin exposures: 15 min (100 nM), approximating to acute stimulation; 48 h (100 nM), used to demonstrate adaptive changes; and 12 weeks (20 nM; chronic insulin exposure, CIE), approximating to chronic hyperinsulinaemia.
|
24068609 |
2014 |
Hyperinsulinism
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Common genetic variants in the insulin receptor substrate 1 (IRS1) gene have been recently associated with insulin resistance and hyperinsulinemia.
|
21747052 |
2011 |
Hyperinsulinism
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We show that Igf1r/Irs1 double mutants do not differ phenotypically from Irs1 single mutants and exhibit hyperinsulinemia, while maintaining normal β cell mass and glucose tolerance.
|
20947509 |
2010 |
Hyperinsulinism
|
0.400 |
Biomarker
|
disease |
CTD_human |
Unlike previously reported T2D risk loci, which predominantly associate with impaired beta cell function, the C allele of rs2943641 was associated with insulin resistance and hyperinsulinemia in 14,358 French, Danish and Finnish participants from population-based cohorts; this allele was also associated with reduced basal levels of IRS1 protein and decreased insulin induction of IRS1-associated phosphatidylinositol-3-OH kinase activity in human skeletal muscle biopsies.
|
19734900 |
2009 |
Hyperinsulinism
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Unlike previously reported T2D risk loci, which predominantly associate with impaired beta cell function, the C allele of rs2943641 was associated with insulin resistance and hyperinsulinemia in 14,358 French, Danish and Finnish participants from population-based cohorts; this allele was also associated with reduced basal levels of IRS1 protein and decreased insulin induction of IRS1-associated phosphatidylinositol-3-OH kinase activity in human skeletal muscle biopsies.
|
19734900 |
2009 |
Hyperinsulinism
|
0.400 |
Biomarker
|
disease |
BEFREE |
Allelic variants of genes encoding components of the insulin pathway, including insulin (INS), insulin receptor (INSR), and insulin receptor substrate-1 and insulin receptor substrate-2 (IRS1 and IRS2) have been associated with hyperinsulinemia and insulin resistance and may, therefore, predict susceptibility to colorectal neoplasia.
|
17416760 |
2007 |
Hyperinsulinism
|
0.400 |
Biomarker
|
disease |
BEFREE |
Insulin increased insulin receptor substrate 1 (IRS-1) tyrosine phosphorylation, IRS-1-associated phosphatidylinositol (PI) 3-kinase activity, and phosphorylation of Akt Ser473 and AS160, a newly described Akt substrate that plays a role in GLUT4 exocytosis, approximately 2.3 fold before treatment.
|
15855334 |
2005 |
Hyperinsulinism
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We conclude the following: 1) physiological hyperinsulinemia induces sustained activation of insulin-signaling molecules in human skeletal muscle; 2) the more distal insulin-signaling components (Akt, GSK-3) are activated much more rapidly than the proximal signaling molecules (IRTK as well as insulin receptor substrate 1 and phosphatidylinositol 3-kinase [Wojtaszewski et al., Diabetes 46:1775-1781, 1997]); and 3) prior exercise increases insulin stimulation of both glucose uptake and glycogen synthase activity in the absence of an upregulation of signaling events in human skeletal muscle.
|
10868952 |
2000 |