Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary lecithin can stimulate bile formation and biliary lipid secretion, particularly cholesterol output in bile. Studies also suggested that the lecithin-rich diet might modify hepatic cholesterol homeostasis and lipoprotein metabolism. Therefore, we examined hepatic activities of 3-hydroxy-3 methylglutaryl coenzyme A reductase "HMG -CoA reductase", cholesterol 7 alpha-hydroxylase and acyl-CoA: cholesterol acyltransferase "ACAT" as well as plasma lipids and lipoprotein composition in rats fed diets enriched with 20% of soybean lecithin during 14 days. We also evaluated the content of hepatic canalicular membrane proteins involved in lipid transport to the bile (all P-glycoproteins as detected by the C 219 antibody and the sister of P-glycoprotein "spgp" or bile acid export pump) by Western blotting. As predicted, lecithin diet modified hepatic cholesterol homeostasis. The activity of hepatic HMG-CoA reductase and cholesterol 7 alpha-hydroxylase was enhanced by 30 and 12% respectively, while microsomal ACAT activity showed a dramatic decrease of 75%. As previously reported from ACAT inhibition, the plasma level and size of very low-density lipoprotein (VLDL) were significantly decreased and bile acid pool size and biliary lipid output were significantly increased. The canalicular membrane content of lipid transporters was not significantly affected by dietary lecithin. The current data on inhibition of ACAT activity and related metabolic effects by lecithin mimic the previously reported effects following drug-induced inhibition of ACAT activity, suggesting potential beneficial effects of dietary lecithin supplementation in vascular disease.
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PMID:Effects of dietary soybean lecithin on plasma lipid transport and hepatic cholesterol metabolism in rats. 1255 76

Disorders concerning the metabolism of plasma and intracellular lipids are hallmarks of atherosclerosis. However, failures in proper control of intracellular cholesterol balance, rather than simple cholesterol overloading due to augmented uptake, could fuel atherogenesis. Therefore, the understanding of atherosclerosis-associated lipid alterations, which feed an inflammatory microenvironment in the arterial wall, requires the meticulous investigation of several aspects of lipid synthesis, uptake and export from cells. In this regard, the presence of reactive cysteines in transcription factors and key enzymes of lipid metabolism may dictate cholesterol accumulation, and therefore the progression of vascular disease. The strong inhibitory effect of cysteine-reactant anti-inflammatory cyclopentenone prostaglandins (CP-PGs) over atherosclerosis progression in vivo (LipoCardium technology) symbolizes a new concept of atherosclerosis and its treatment. Results from this laboratory and those from other research groups have unraveled a novel facet in prostaglandin research in that CP-PGs may act as redox signals that guide lipid metabolism in atherosclerosis. By modifying enzymes (e.g., HMG-CoA reductase, ACAT and cholesteryl ester hydrolases) and transcription factors (e.g., NF-kappaB and Keap1) involved in inflammation and lipid metabolism, CP-PGs (especially those of A-series) induce pivotal changes in glutathione and lipid metabolism that completely arrest atherosclerosis progression. Hence, pharmacological manipulation of lipid metabolism by CP-PGs may be a novel and invaluable strategy for treating atherosclerosis. Also, a better understanding of why CP-PGs do not resolve inflammation physiologically may explain many unsolved questions and yield insights into atherogenesis and its termination.
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PMID:Atherosclerosis: a redox-sensitive lipid imbalance suppressible by cyclopentenone prostaglandins. 1844 Apr 92