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scurvy/triglyceride
Veza se sprema u međuspremnik
12 rezultatima
The effect of chronic marginal vitamin C deficiency on the rate of secretion and the removal of plasma triglycerides in guinea-pigs.
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In guinea-pigs, chronic borderline vitamin C deficiency leads to hypertriglyceridaemia and to the accumulation of triglycerides in the liver. We investigated the triglyceride secretion rate by determining the rate of accumulation of triglycerides in the plasma following a Triton WR 1339 block of the
Effect of long-term marginal vitamin C deficiency on plasma triglyceride kinetics in guinea-pigs.
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A multicompartmental analysis of the plasma triglyceride kinetics after [3H]glycerol administration revealed that hypertriglyceridemia in vitamin c deficient guinea-pigs was caused by a slowed triglyceride removal from the plasma compartment.
[Post-heparin lipolytic activity of plasma, secretion rate of triglycerides and kinetics of plasma triglycerides in guinea pigs with chronic borderline vitamin C deficiency].
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Serum triglycerides and post-heparin lipolytic activity in guinea-pigs with latent vitamin C deficiency.
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The influence of chronic vitamin C deficiency on fatty acid composition of blood serum, liver triglycerides and cholesterol esters in guinea pigs.
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Aggravation of cholesterol induced hyperlipidemia by chronic vitamin C deficiency: experimental study in guinea pigs.
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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
Effect of vitamin C deficiency and excess on the liver: a histopathological and biochemical study in guinea pigs fed normal or high cholesterol diet.
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When guinea pigs were kept on a restricted vitamin C intake of only 0.5 mg daily, their serum ascorbic acid fell to 0.16 +/- 0.06 mg/d1 in 16 weeks as compared to 0.73 +/- 0.11 in control. This was associated with significant increase in liver cholesterol and triglycerides. When they were
The role of ascorbic acid in the regulation of cholesterol metabolism and in the pathogenesis of artherosclerosis.
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Strong clinical and experimental evidence suggests that chronic latent vitamin C deficiency leads to hypercholesterolaemia and the accumulation of cholesterol in certain tissues. Ascorbic acid supplementation of the diet of hypercholesterolaemic humans and animals generally results in a significant
Effect of vitamin C depletion on serum cholesterol and lipoprotein levels in ODS (od/od) rats unable to synthesize ascorbic acid.
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The effect of ascorbic acid deficiency on serum and liver cholesterol, phospholipid and triglyceride levels, serum lipoprotein levels and serum lipoprotein cholesterol levels were examined in male rats with a hereditary defect in ascorbic acid synthesis (ODS rats). Male homozygotes (od/od) and male
No effect on serum lipids by moderate and high doses of vitamin C in elderly subjects with low plasma ascorbic acid levels.
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The influence of dietary supplementation with moderate (200 mg/day) and high (2,000 mg/day) doses of vitamin C on serum lipid levels was studied in 27 female long-stay hospital patients characterized by low plasma ascorbic acid levels during the preceding year. The two doses of vitamin C were
Lack of antiscorbutic activity of ascorbate 2-sulfate in the rhesus monkey.
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Oral administration of 10 mg per kilogram of body weight of ascorbic acid (AA) completely prevented development of scurvy in juvenile rhesus monkey (Mucaca mulata) fed an AA-free liquid diet. The same dose cured scurvy when injected intramuscularly. An equimolar dose of ascorbic acid 2-sulfate
Lack of effect of experimental ascorbic acid deficiency on bile acid metabolism, sterol balance, and biliary lipid composition in man.
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Extensive studies in animal models indicate that subclinical ascorbic acid deficiency impairs the conversion of cholesterol to bile acid, elevates plasma cholesterol levels, and predisposes to development of cholesterol cholelithiasis. The present study was designed to see if this is also true in
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