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Am J Physiol Endocrinol Metab 279: E1003-E1011, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 5, E1003-E1011, November 2000

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

Doru V. Chirieac*, Lucian R. Chirieac*, James P. Corsetti, Joanne Cianci, Charles E. Sparks, and Janet D. Sparks

Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642

The current study assessed in vivo the effect of insulin on triglyceride-rich lipoprotein (TRL) production by rat liver. Hepatic triglyceride and apolipoprotein B (apoB) production were measured in anesthetized, fasted rats injected intravenously with Triton WR-1339 (400 mg/kg). After intravascular catabolism was blocked by detergent treatment, glucose (500 mg/kg) was injected to elicit insulin secretion, and serum triglyceride and apoB accumulation were monitored over the next 3 h. In glucose-injected rats, triglyceride secretion averaged 22.5 ± 2.1 µg · ml-1 · min-1, which was significantly less by 30% than that observed in saline-injected rats, which averaged 32.1 ± 1.4 µg · ml-1 · min-1. ApoB secretion was also significantly reduced 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 hepatic very low density lipoprotein (VLDL) triglyceride and apoB secretion and strengthen the concept of a regulatory role for insulin in VLDL metabolism postprandially.

lipoprotein secretion by liver; very low density lipoprotein; Triton WR-1339 treatment; in vivo apolipoprotein B production

* D. V. Chirieac and L. R. Chirieac contributed equally to this work.




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