Enhancement of beta-cell sensitivity to glucose by oral fat load

Recent studies have demonstrated that 6 In infusions of lipid emulsion enha nce insulin release, whereas 24 h infusions inhibit insulin secretion. How insulin release is modulated after oral fat loading has not yet been elucid ated. 17 healthy fasting volunteers were subjected to 3 experiments in rand om order: test 1 was a frequently sampled Lv. glucose tolerance test (FSIVG TT, 0.3 g/kg glucose), test 2 began with the ingestion of 50% sunflower oil (1.5 g/kg) followed by FSIVGTT 4 In later. Test 3 was identical to test 2 with Lv. addition of 100 IU/kg heparin prior to FSIVGTT. Glucose and insuli n data were analyzed by minimal model assumptions - glucose sensitivity of the beta -cells (Theta1), acute insulin response (AIR) (10 min), 3 In insul in release (Theta2), glucose threshold of insulin secretion (h), insulin de gradation rate (n), peripheral insulin sensitivity (S-I), and glucose-depen dent glucose disposal (SG). After drinking the fat emulsion, FFAs increased to 0.8 +/- 0.3 mmol/l (test 2) and to 3.0 +/- 0.3 mmol/l (test 3). Moderat ely increased FFA concentrations were associated with elevation of Theta1 ( test 1, control 335 +/- 157 vs. test 2: 859 +/- 612 pM x min x mM(-1). p = 0.030). At high plasma FFA levels and in the presence of heparin (test 3), Theta1 was reduced compared to test 2 and unchanged compared to test 1. The ta2 and h were elevated in both tests 2 and 3 compared to test 1. No change s of n, S-I and S-G were found. In conclusion, the ingestion of sunflower o il triglycericle emulsion resulted in a 60% increase in plasma free fatty a cids and enhanced the capacity of beta -cells to secrete insulin. Heparin-i nduced high levels of FFA further augmented the total insulin release and i nhibited parameters of glucose responsiveness.