Course Of Glucose Tolerance Test Research Articles

Role of Peroxisome Proliferator-activated Receptor δ/β in Hepatic Metabolic Regulation

Pharmacological activation of peroxisome proliferator-activated receptor δ/β (PPARδ/β) improves glucose handling and insulin sensitivity. The target tissues of drug actions remain unclear. We demonstrate here that adenovirus-mediated liver-restricted PPARδ activation reduces fasting glucose levels in chow- and high fat-fed mice. This effect is accompanied by hepatic glycogen and lipid deposition as well as up-regulation of glucose utilization and de novo lipogenesis pathways. Promoter analyses indicate that PPARδ regulates hepatic metabolic programs through both direct and indirect transcriptional mechanisms partly mediated by its co-activator, PPARγ co-activator-1β. Assessment of the lipid composition reveals that PPARδ increases the production of monounsaturated fatty acids, which are PPAR activators, and reduces that of saturated FAs. Despite the increased lipid accumulation, adeno-PPARδ-infected livers exhibit less damage and show a reduction in JNK stress signaling, suggesting that PPARδ-regulated lipogenic program may protect against lipotoxicity. The altered substrate utilization by PPARδ also results in a secondary effect on AMP-activated protein kinase activation, which likely contributes to the glucose-lowering activity. Collectively, our data suggest that PPARδ controls hepatic energy substrate homeostasis by coordinated regulation of glucose and fatty acid metabolism, which provide a molecular basis for developing PPARδ agonists to manage hyperglycemia and insulin resistance.

Prediction of hyperkalemia associated with prolonged treatment with captopril by glucose-induced acute serum potassium changes.

The effect on potassium levels of short-term (5-10 days) and "prolonged" (4 weeks) captopril therapy were compared. No consistent changes during short-term treatment were found and the elevations in serum potassium associated with prolonged treatment could not be predicted on the basis of short-term changes. However, a definite correlation was found between glucose-induced serum potassium alterations (in the course of glucose tolerance test) during short-term captopril administration and elevations in baseline serum potassium during prolonged treatment In the patients with glucose-induced paradoxical serum potassium elevations, baseline serum potassium levels increased more markedly during prolonged captopril therapy than in patients with the opposite glucose-induced changes.