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.
D000818:Animals; D001059:Apoproteins / Q000378:metabolism; D004195:Disease Models, Animal; D006949:Hyperlipidemias / Q000139:chemically induced*; D007413:Intestinal Mucosa / Q000378:metabolism*; D008079:Lipoproteins, VLDL / Q000378:metabolism*; D008297:Male; D011092:Polyethylene Glycols / Q000494:pharmacology*; D051381:Rats; D014280:Triglycerides / Q000097:blood* / Q000378:metabolism
D001059:Apoproteins; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D011092:Polyethylene Glycols