Glucose-stimulated insulin secretion suppresses hepatic triglyceride-rich lipoprotein and apoB production

The current study assessed in vivo the effect of insulin on triglyceride-ri ch lipoprotein (TRL) production by rat liver. Hepatic triglyceride and apol ipoprotein B (apoB) production were measured in anesthetized, fasted rats i njected intravenously with Triton WR-1339 (400 mg/kg). After intravascular catabolism was blocked by detergent treatment, glucose (500 mg/kg) was inje cted to elicit insulin secretion, and serum triglyceride and apoB accumulat ion were monitored over the next 3 h. In glucose-injected rats, triglycerid e secretion averaged 22.5 +/- 2.1 mug.ml(-1).min(-1), which was significant ly less by 30% than that observed in saline-injected rats, which averaged 3 2.1 +/- 1.4 mug.ml(-1)min(-1). ApoB secretion was also significantly reduce d by 66% in glucose-injected rats. ApoB immunoblotting indicated that both B100 and B48 production were significantly reduced after glucose injection. Results support the conclusion that insulin acts in vivo to suppress hepat ic very low density lipoprotein (VLDL) triglyceride and apoB secretion and strengthen the concept of a regulatory role for insulin in VLDL metabolism postprandially.