Abstract
Monomethylethanolamine (MME) inhibits very low density lipoprotein (VLDL) secretion from cultured rat hepatocytes by disruption of translocation of apolipoprotein (apo) B across the endoplasmic reticulum membrane (A. E. Rusiñol, E. Y. W. Chan and J. E. Vance. 1993. J. Biol. Chem. 268: 25168-25175). We have now investigated whether or not plasma levels of lipids and apoB are reduced by dietary supplementation of rats with MME. In rats fed MME for 5 to 7 days, the levels of triacylglycerols and apoB in VLDL were reduced by 66% and 45%, respectively. At the same time, MME feeding also increased plasma apoA-I by 80%. No significant differences were found in body or liver weights between control and MME-fed rats, nor did the reduction of plasma VLDL in MME-fed rats result in accumulation of triacylglycerols in the liver. When the dietary period was extended to 15 weeks, essentially the same results were obtained except that plasma cholesterol was increased by 31% in MME-treated animals, apparently because of increased amounts of apoA-I and high density lipoproteins. According to post-mortem and microscopic examination, rats fed MME for 15 weeks were anatomically normal with no indication of any lipid accumulation in the liver. The ability of MME to reduce VLDL secretion and at the same time to increase the level of high density lipoproteins are attractive properties of a therapeutic agent for treatment of atherosclerosis in humans.
Highlights
Monomethylethanolamine (MME) inhibits very low density lipoprotein (VLDL) secretion from cultured rat hepatocytes by disruption of translocation of apolipoprotein B across the endoplasmic reticulum membrane
This study demonstrates that dietary supplementation of rats with MME for as little as 5 days markedly reduced plasma lipids, in particular VLDL triacylglycer01s which were reduced by 66%
The reduction in the triacylglycerol content of plasma was accompanied by an almost parallel decrease in the amount of plasma apoB. These data indicate that the number of plasma VLDL particles was reduced in rats fed MME. These observations in intact rats support our previous finding that when cultured primary rat hepatocytes were incubated with MME the secretion of VLDL lipids and apoproteins was reduced by 50-70% [11, 13].The VLDL-lowering effect of MME did not appear to be detrimental to the growth or health of the animals as no significant differences in body or liver weight were detected between the two groups of rats
Summary
Monomethylethanolamine (MME) inhibits very low density lipoprotein (VLDL) secretion from cultured rat hepatocytes by disruption of translocation of apolipoprotein (apo) B across the endoplasmic reticulum membrane According to post-mortem and microscopic examination, rat fed MME for 15weeks were anatomically normal with no indication of any lipid accumulation in the 1iver.l The ability of MME to reduce VLDL secretion and at the same time t o increase the level of high density lipoproteins are attractive properties of a therapeutic agent for treatment of atherosclerosis in humans.-Rusiiiol, A. Many recent studies have suggested that translocation of apoB across the endoplasmic reticulum membrane, perhaps in conjunction with assembly of the protein with lipids, might be an important regulatory step in VLDL secretion [9,10,11,12].
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