Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic vitamin C deficiency was induced in guinea pigs by restricting their vitamin C intake to 0.5 mg daily. This was just sufficient to prevent rapidly fatal scurvy and 55 per cent of the animals survived. In 16 weeks their serum ascorbic acid (SAA) fell to 0.16 +/- 0.06 mg/dl as compared to 0.73 +/- 0.11 in control animals receiving 5 mg vitamin C daily. There was a marked increase in serum cholesterol, LDL-cholesterol, VLDL-cholesterol, triglycerides and total lipids. HDL-cholesterol was, however, decreased resulting in a shift of the LDL/HDL ratio from 1.13 +/- 0.16 in the control to 5.91 +/- 1.70 in the low vitamin C group. Cholesterol feeding (100 mg/day) by itself lowered the SAA significantly, besides producing hyperlipidemia. When the vitamin C intake was reduced to only 0.5 mg/day, the effects of cholesterol feeding were exaggerated; the magnitude of hyperlipidemia was now significantly greater than with simple cholesterol feeding. The LDL/HDL ratio rose to 19.02 +/- 3.32 from 1.13 +/- 0.16 in the normal guinea pigs. Chronic vitamin C deficiency seems to affect the blood lipid profile unfavourably which could promote atherogenesis.
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PMID:Aggravation of cholesterol induced hyperlipidemia by chronic vitamin C deficiency: experimental study in guinea pigs. 325 10

A study was made of hyperlipidemia caused by ascorbic acid deficiency and of the effects of cholesterol, DL-ethionine and aflatoxin on plasma lipoprotein fractions of normal and scorbutic guinea pigs. The plasma lipoprotein fractions of scorbutic animals showed a significantly higher level of pre-beta-lipoprotein and a lower level of alpha-lipoprotein. By adding DL-ethionine to the control group, the pre-beta-lipoprotein fraction was remarkably elevated and by adding cholesterol, the alpha-lipoprotein level was greatly reduced and the beta-lipoprotein level was increased. Addition of aflatoxin to the control diet resulted in a rather high concentration of alpha-lipoprotein and a low pre-beta-lipoprotein level. High concentrations of triglyceride and phospholipid were seen in the plasma of scorbutic guinea pigs. The probable cause of hyperlipidemia induced by ascorbic acid deficiency is partly retarded degradation of cholesterol resulting from impaired 7 alpha-hydroxylation, and partly that ascorbic acid deficiency may affect other enzyme systems that control triglyceride of phospholipid metabolism, such as lipoprotein lipase activity, or synthesis or breakdown of these enzymes.
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PMID:Hyperlipidemia in guinea-pigs induced by ascorbic acid deficiency. The effects of cholesterol, DL-ethionine and aflatoxin. 722 63

Effects of L-ascorbate 2-sulfate (AAS) on fatty liver and hyperlipidemia induced by various treatments were studied in rats and guinea pigs. L-Ascorbic acid (AA) (50 or 175 mg/kg), a reference compound, lowered the lipid levels in the serum and/or liver in guinea pigs, while AA had little effect in rats. On the other hand, AAS (300 mg/kg) was effective in both animals. In rats, AAS lowered cholesterol and triglycerides in the serum from ethionine-treated animals and in the liver from orotic acid-supplemented animals. In guinea pigs, this compound lowered cholesterol and triglycerides in the serum from ethionine-treated animals, lipids in the liver from cholesterol-supplemented animals, and lipids in the serum and liver from scorbutic animals. AA markedly increased the content of AA in the organs in all experiments, while AAS had a slight effect. Thus, it is suggested that AAS exerts its hypolipidemic and lipotropic effects by the specific actions of AAS.
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PMID:Effect of l-ascorbate 2-sulfate on fatty liver and hyperlipidemia induced by various treatments in rats and guinea pigs. 724 Dec 35