Prompted by the reported hypolipidemic activity of garlic, the present study was undertaken to elucidate the mechanism(s) underlying the cholesterol-lowering effects of garlic. Rat hepatocytes in primary culture were used to determine the short-term effects of garlic preparations on [1-14C]acetate and |2-3H]glycerol incorporation into cholesterol, fatty acids and glycerol lipids. When compared with the control group, cells treated with a high concentration of garlic extracts [i.e., petroleum ether-(PEF), methanol-(MEF) and water-extractable (WEF) fractions from fresh garlic] showed decreased rates of [1-14C]acetate incorporation into cholesterol (by 37-4i4%) and into fatty acids (by 28-64%). Kyolic containing S-allyl cysteine and organosulfur compounds inhibited cholesterogenesis in a concentration dependent manner with a mn~dmum inhibition of87% at 0.4 raM. At this concentration, Kyolic decreased [1-14C]acetate incorporation into fatty acids by 67%. Sallyl cysteine at 2.0 and 4.0 mM inhibited cholesterogenesis by 20-25%. PEF, MEF and WEF depressed the rates of [2-3H]glyeerol incorporation into triacylglycerol, diacylglycerol and phospholipids in the presence of acetate, but not in the presence of oleate. The results suggest that the hypocholesterolemic effect of garlic stems, in part, from decreased hepatic cholesterogenesis, whereas the triacylglycerol-lowering effect appears to be due to inhibition of fatty acid synthesis. Primary hepatocyte cultures as used in the present study have been proven useful as tools for screening the anticholesterogenie properties of garlic principles.Lipids 29, 189-193 (1994).Aside from its general use as a condiment, garlic (A1lium sativum) is known for its pharmacological and nutritional properties (1). Among the potential therapeutic applications of garlic, its antilipidemic effects have been demonstrated in studies on humans (2-6), as well as on animals, including rats (7-13), rabbits (14,15), chicken (16-17) and swine (18). Garlic is known to contain a variety of sulfur compounds, in addition to amino acids, vitamins and minerals (19). Although some of these sulfur compounds, such as S-methylcysteine sulfoxide and Sallyl cysteine sulfoxide, are known to reduce cholesterol levels in the liver and plasma (10), the principle(s) foremost responsible for the hypolipidemic action of garlic is presently not known. Likewise, the mechanism(s) underlying the hypocholesterolemic effects of garlic constituents(s) have not been fully elucidated (20).
We investigated hypohomocysteinemic action as a cardiovascular protective property of aged garlic extract (AGE). Hyperhomocysteinemia was induced in rats by feeding folate-depleted diets. Plasma folate concentrations of 5, 24, and 202 nmol/L were detected in rats fed a folate-deficient L-amino acid diet containing succinyl sulfathiazole, an AIN-93G folate-deficient diet, and an AIN-93G folate-sufficient diet, respectively. Plasma concentrations of total homocysteine were elevated to the highest level (32 micromol/L) by severe folate deficiency and to a moderate level (9 micromol/L) by mild folate deficiency, compared with the lowest level of (5 micromol/L), noted for the folate-sufficient group. The addition of AGE to the severely folate-deficient diet decreased plasma total homocysteine concentration by 30%. Hyperhomocysteinemia caused by mild folate deficiency remained unaltered by AGE supplementation. The reduction in total homocysteine of the severely folate-deficient rats was accompanied by a proportional decrease in protein-bound and free homocysteine, resulting in an unchanged protein-bound:free homocysteine ratio. AGE added to the diet did not alter plasma concentrations of other aminothiol compounds: cysteine, glutathione, and cysteinylglycine. These data, together with increased S-adenosylmethionine and decreased S-adenosylhomocysteine concentrations in the liver, suggest that the hypohomocysteinemic effect of AGE most likely stems from impaired remethylation of homocysteine to methionine and enhanced transsulfuration of homocysteine to cystathionine. More importantly, in addition to its cholesterol-lowering potential, blood pressure-lowering effect, and antioxidant property, a hypohomocysteinemic action may be another important cardiovascular protective factor of AGE.
The study was undertaken to determine whether the content of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in neonatal rats can be increased through milk provided by lactating mothers fed a diet containing 20% menhaden oil (experimental group), in comparison with a group fed a 20% corn oil diet (control group). The test diets were isocaloric and provided 41% of total energy as fat. Coinciding with 3-9% higher maternal body weight gain throughout the lactation period with the menhaden oil diet, the suckling rats in the experimental group at the ages of 3-9 d gained 5-10% more weight than did their control counterparts. When compared with corn oil, maternal dietary menhaden oil induced not only a higher weight percentage but also higher concentrations (microgram/mL) of EPA, DHA and total (n-3) fatty acids in milk, plasma, platelets and erythrocytes of neonates. These changes were accompanied by lower arachidonic and linoleic acid levels. EPA and DHA were detected in all three blood components of the control group, whose corn oil diet contained linolenic acid but not longer chain (n-3) fatty acids. This finding, together with the higher DHA to EPA ratios found in the three blood components than in the milk of the experimental group, suggests that neonatal rats possess the enzymes necessary for producing DHA from EPA and linolenate by desaturation and elongation mechanisms.
Prompted by the speculated essentiality of docosahexaenoic acid (DHA) for neural development, this study was undertaken to investigate the incorporation of (n-3) fatty acids in the maternal diet into various phospholipids of infant rat brain subcellular fractions: microsomes (Ms), synaptosomes (Sy), myelin (My), and mitochondria (Mt). Two groups of infant rats were nourished by dams fed diets containing 20% of either corn oil (CO) or menhaden oil (MO) from 2 until 12 days of age. DHA but not eicosapentaenoic acid (EPA) was distributed to all subcellular fractions of infant rats in the CO group. The levels of DHA were higher in Ms and Mt than Sy and My, and higher in phosphatidylethanolamine (PE) and phosphatidylserine (PS) than phosphatidylcholine (PC) and phosphatidylinositol (PI). The MO feeding enriched DHA in PE of all subcellular fractions, PS of all subcellular fractions, except My, PC of Sy, My and Mt, and PI of My. EPA was enriched in phospholipids in all subcellular fractions, except mitochondrial PS of the MO group. In the MO group, the ratios of EPA/DHA, ranging from 0.01 to 0.85, in all subcellular phospholipids were markedly lower than that found in the mother's milk (i.e., 1.5), suggesting an ability to elongate and desaturate EPA to DHA and/or disproportional uptake of the fatty acids by the brain. In PE of all subcellular fractions, the increased levels of DHA and EPA, with a concomitant reduction of arachidonic and/or linoleic acid, yielded higher ratios of total (n-3)/(n-6) fatty acids in the MO than the CO group. The inclusion of preformed DHA and EPA in the maternal diet provides an effective means to enrich these fatty acids in developing brains.
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