Triton-induced hyperlipidemia: a model for studies of intestinal lipoprotein production.

To estimate intestinal very low-density lipoprotein (VLDL) contribution to the circulating plasma triglyceride (TG) pool, mesenteric, hepatic, and total TG production rates were measured in mesenteric lymph-cannulated male rats after Triton WR-1339 blockage of systemic VLDL metabolism. The intestinal contribution (4.92 +/- 0.5 mg TG/h) was calculated to be 19% of total TG production rate. Triton WR-1339 administration caused profound hyperlipoproteinemia but did not alter total lymph TG or VLDL apoprotein output. The percent of lymph VLDL apoprotein present as apo A-I and apo A-IV fell dramatically after Triton with a concomitant increase in apo E and apo C peptides. Studies in this Triton-treated rat model suggest that the intestinal contribution to systemic TG formation is small but that changes in circulating apolipoproteins may alter the composition of intestinal VLDL.