<b>Results:</b> Addition of ApoA-I produced cAMP and increased insulin secretion, dose-dependently in high glucose concentration (25 mmmol/l). and ABCA1 protein and Cdc42 mRNA and protein were also enhanced.
<b>Results:</b> Addition of ApoA-I produced cAMP and increased insulin secretion, dose-dependently in high glucose concentration (25 mmmol/l). and ABCA1 protein and Cdc42 mRNA and protein were also enhanced.
(iv) The interference of a physiological response to insulin by ACE inhibitors or beta-blocking agents may have implications both for energy balance and thermoregulation during periods of hyperinsulinaemia in man.
Insulin increasedGYS1 messenger ribonucleic acid (mRNA) expression in control subjects (from 0.14 +/- 0.02 to 1.74 +/- 0.10 relative units; P < 0.01) and in nondiabetic (from 0.24 +/- 0.05 to 1.81 +/- 0.16 relative units; P < 0.01) and diabetic (from 0.20 +/- 0.07 to 1.08 + 0.14 relative units; P < 0.01) twins.
Insulin increased Akt serine phosphorylation in control subjects and IGT relatives, with a tendency for reduced phosphorylation in IGT relatives (P = 0.12).
Insulin increasedinsulin 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.
Hyperinsulinemia and impaired leptin-adiponectin ratio associate with endothelial nitric oxide synthase polymorphisms in subjects with in-stent restenosis.
Hyperinsulinism/ hyperammonemia (HI/HA) syndrome is caused by excessive activity of glutamate dehydrogenase (GDH) encoded by GLUD1 gene, which oxidizes glutamate to alpha-ketoglutarate and which is a potential regulator of insulin secretion in pancreatic beta cells and of ureagenesis in the liver.
Hyperinsulinemia associated with non-ketotic hypoglycemia is observed in patients with mutated β-oxidation enzyme short-chain 3-hydroxyacyl-CoA dehydrogenase (HADHSC).
Hyperinsulinemia, associated with partial lipodystrophy, elevated RBP4, low adiponectin levels, and decreased expression of GLUT3 and GLUT4 were detected.
Hyperinsulinemia, associated with partial lipodystrophy, elevated RBP4, low adiponectin levels, and decreased expression of GLUT3 and GLUT4 were detected.
Hyperinsulinaemia and hyperglycaemia exerted independent effects with similar direction of modulation on PI3KR1 (phosphatidylinositol 3-kinase, regulatory 1), LXRα (liver X receptor α), PDK4 (pyruvate dehydrogenase kinase 4) and FOXO1 (forkhead box O1A) and produced an additive effect on PI3KR1, the gene that encodes the p85α subunit of PI3K in human skeletal muscle.