References: Lecithin
Hepatology. 1992 Mar;15(3):373-81.
Polyunsaturated lecithin prevents acetaldehyde-mediated hepatic collagen accumulation by stimulating collagenase activity in cultured lipocytes.
Li J, Kim CI, Leo MA, Mak KM, Rojkind M, Lieber CS.
Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center, New York.
We recently found that polyunsaturated lecithin prevents ethanol from causing cirrhosis in the baboon. Because transformation of lipocytes to transitional cells plays a key role in hepatic fibrogenesis in vivo, and because this process in alcohol-fed baboons was found to be attenuated by polyunsaturated lecithin, we focused on lipocytes to study the mechanism of the protective effect. Rat lipocytes cultured on plastic undergo spontaneous activation, accompanied by expression of alpha-smooth muscle actin isoform and production of substantial amounts of type I collagen. The latter was further increased on incubation with acetaldehyde. This in vitro model was used here to study how acetaldehyde-mediated collagen production and accumulation can be turned off. Addition of polyunsaturated lecithin (10 mumols/L) was found to prevent the acetaldehyde-induced increase in collagen accumulation by 83% (p less than 0.001). By contrast, a saturated phospholipid (10 mumols/L dilauroyl phosphatidylcholine), a monounsaturated one (10 mumols/L linoleoyl-palmitoyl phosphatidylcholine) or linoleic acid (20 mumols/L bound to albumin) had no such effect. Incorporation of [3H]proline into collagen and the expression of alpha-1 (I) procollagen mRNA were increased by acetaldehyde; the latter was not significantly affected by polyunsaturated lecithin. Polyunsaturated lecithin increased lipocyte collagenase activity by 100% (p less than 0.001), whereas dilauroyl phosphatidylcholine, linoleoyl-palmitoyl phosphatidylcholine and linoleic acid had no such action. We concluded that (a) polyunsaturated lecithin selectively prevents the acetaldehyde-induced increase in collagen accumulation in lipocyte c
Cancer Res. 1993 Jul 1;53(13):2965-9.
Effects of pharmacological retinoids on several vitamin A-metabolizing enzymes.
Dew SE, Wardlaw SA, Ong DE.
Vanderbilt University School of Medicine, Department of Biochemistry, Nashville, Tennessee 37232.
Fenretinide (HPR), 13-cis-retinoic acid, and all-trans-retinoic acid are vitamin A derivatives used in the treatment of cancer and severe acne. Patients taking these drugs often show side effects resembling the symptoms of hypovitaminosis A, namely, night blindness and decreased plasma retinol levels. A dietary vitamin A deficiency is not suspected in these patients; therefore, interference with normal vitamin A metabolism seems likely. The effect of these drugs on two enzymes involved in vitamin A metabolism was investigated. At micromolar concentrations, all three derivatives were found to inhibit intestinal lecithin-retinol acyltransferase (LRAT) and to a lesser extent liver LRAT and intestinal retinal reductase. Inhibition of intestinal LRAT by HPR and 13-cis-retinoic acid was enhanced by preincubation prior to assay, whereas inhibition of the other activities was not. The Ki for the inhibition of intestinal LRAT by HPR was determined to be 24.1 +/- 5.6 microM. The ability of these drugs to inhibit retinal reduction and retinol esterification in vitro suggests an ability to interfere with normal vitamin A metabolism in vivo, particularly during absorption. This may be most significant for HPR, which is known to accumulate in the liver and intestine after chronic dosing.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8319203&dopt=Abstract lecithin
Metabolism. 1988 Jun;37(6):535-41.
The acute effect of prolonged walking and dietary changes on plasma lipoprotein concentrations and high-density lipoprotein subfractions.
Griffin BA, Skinner ER, Maughan RJ.
Department of Biochemistry, University of Aberdeen, Scotland.
The effect of diet on exercise-induced changes in the plasma concentrations of lipoproteins was examined in six healthy male subjects during walks of 37 km on each of four successive days. With a high-carbohydrate diet (85% of the calories as carbohydrate) there was an increase (P less than .05) in the concentration of very-low-density lipoprotein (VLDL)-cholesterol and VLDL-triglyceride and a decrease (P less than .01) in the concentration of high density lipoprotein (HDL)-cholesterol, due mainly to a decrease in HDL3-cholesterol (P less than .01), and HDL-protein (P less than .001). In contrast, a high-fat diet (75% fat) produced a decrease (P less than .01) in the concentration of VLDL-cholesterol and VLDL-triglyceride with increases (P less than .01) in HDL-protein concentration and in HDL-cholesterol concentrations that arose largely from an increase (P less than .001) in HDL2-cholesterol. Gradient gel electrophoretic analysis showed an increase (P less than .01) in the relative concentration of HDL2b (subspecies of diameter 10.57 nm) with a decrease (P less than .01) in the concentration of HDL2a (9.16 nm) plus HDL3a (8.44 nm) with the high-fat diet, but no significant or consistent change with the high-carbohydrate diet. There was no change in the level of the apolipoprotein E-rich HDL subfraction with either diet. Plasma lecithin:cholesterol acyltransferase activity decreased (P less than .05) with the high-fat diet but not with the high-carbohydrate diet. Thus, diet can strongly influence the changes that occur in plasma lipoprotein concentrations during prolonged low-intensity exercise.
Laxative online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3163762&dopt=Abstract lecithin
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