Monomethylethanolamine reduces plasma triacylglycerols and apolipoprotein B and increases apolipoprotein A-I rats without induction of fatty liver.

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.