Possible Interaction: Glucose and Insulin

“Incremental AUCs (AUCincr) of glucose and insulin tended to increase (41% increase in glucose AUCincr, P = 0.21, 95% confidence interval (CI) of the difference -47, 187; 24% increase in insulin AUCincr, P = 0.084, CI of the difference -110, 1493).”

“In study 3 (intensified insulin treatment), intensification of glucose control with insulin resulted in a concomitant and parallel reduction of average weekly glucose and GCD59 within 2 weeks.”

“….Insulin … glucose infusion led to the maintenance of euglycemia and a significant suppression of reactive oxygen species (ROS) generation, p47(phox) expression, Toll-like receptor (TLR)-… adhesion molecule expression and a fall in serum concentrations of C-reactive protein, HMGB1, and rapid upon activation T cell expressed and secreted.”

“RESULTS After D- lc in fusion, plasma ins ulin co ncentrations increased significantly (period I, 6.6 ± 1.8 µU/mL; period II, 21.4 ± 2.1 µU/mL; P < .01).”

“ Insulin suppression of hepatic glucose output improved from 43 ± 4% to 74 ± 5% (p = 0.003 vs baseline; controls 68 ± 5%).”

“Preexposure to exogenous insulin increased the endogenous insulin secretory response to glucose by ≈40%.”

“Although blood glucose remained stable after initiation of insulin infusion, insulin induced a significant decrease in cerebral glucose at 3 hours after onset of the infusion until the end of the observation period (P < 0.05), reflecting high glucose utilization.”

“Though no insulin-induced hypoglycemia occurred, cerebral glucose decreased on days 1–4 after insulin onset without reaching critical levels.”

“Furthermore, oral glucose loading during recovery increased plasma insulin markedly more in F (+46.80 μU ml−1) than in CHO (+14.63 μU ml−1, P= 0.02).”

“The administration of glucose caused an increase in the circulating concentration of insulin (P < 0.05) resulting in a lower glucagon/insulin quotient than in the control group (P < 0.05).”