PubMed · 2270018
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S Koga. 1990. [Endogenous (type IV) hypertriglyceridemia].. https://pubmed.ncbi.nlm.nih.gov/2270018/
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The objective of this study was to examine the effect of insulin on lipoprotein synthesis and secretion in human fetal intestine. Jejunal explants were cultured with [14C]oleic acid in Leibovitz medium for 42 h. Although the addition of insulin (30 U) did not alter the incorporation of [14C]oleic acid into triglycerides, phospholipids and cholesteryl esters in the tissue, it significantly decreased (P < 0.05) the level of triglycerides (20%) in the medium. Among the three lipoprotein classes (chylomicron, VLDL, and HDL) isolated by ultracentrifugation, the chylomicron level was found significantly (P < 0.05) diminished in the medium (29%). Neither the lipid chemical composition of CM or that of VLDL, LDL and HDL was affected by the presence of insulin. These results suggest that chylomicron synthesis is modulated by insulin, whereas lipoprotein distribution and lipid composition are not regulated by this hormone.
Trauma, thermal injury, and nonlethal doses of endotoxin can promote the translocation of endotoxin across the mucosal barrier of the colon into the mesenteric lymphatics and systemic circulation. Bacterial endotoxemia induces changes in lipid metabolism, including an increase in circulating triglyceride-rich lipoproteins. Because cholesterol-rich lipoproteins can neutralize the toxic activity of endotoxin, both in vitro and in vivo, we asked whether triglyceride-rich chylomicrons can inhibit endotoxin activity in vitro as measured by a chromogenic Limulus assay. We tested the effect of intact versus heat-denatured chylomicrons on the in vitro activity of increasing concentrations of Escherichia coli (055:B5) endotoxin. Intact chylomicrons inhibited up to 12-fold the detection of as much as 1 microgram of endotoxin/mg of chylomicron triglyceride, compared to denatured chylomicrons (P less than 0.001). This study shows that chylomicrons are potent inhibitors of endotoxin activity in vitro. Because translocated endotoxin from the colon associates with gut-derived chylomicrons in the mesenteric lymphatics, this may represent a natural defensive mechanism against endotoxemia of enteric origin.
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