Relationship between Cholesterol and Vitamin a Metabolism in Rats Fed at Different Levels of Vitamin A

Bring, Shirley V.; Ricard, Cecelia A.; Zaehringer, Mary V.

doi:10.1093/jn/85.4.400

Cited by 17 publications

(3 citation statements)

References 16 publications

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“…Similar observations have been made on serum cholesterol level of chicks made hypercholesterolemic by the addition of cholesterol to the diet (Wood, 1960). Quite recently, Bring et al (1965) reported an inverse relationship between vitamin A and cholesterol content of serum and liver in rats fed diets containing added cholesterol.…”

Section: Effect Of Dietary Vitamin a And Cholesterol On Cholesterol Asupporting

confidence: 76%

Effect of Dietary Vitamin A and Cholesterol on Cholesterol and Carotenoid Content of Plasma and Egg Yolk

et al. 1967

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Section: Effect Of Dietary Vitamin a And Cholesterol On Cholesterol Asupporting

confidence: 76%

Effect of Dietary Vitamin A and Cholesterol on Cholesterol and Carotenoid Content of Plasma and Egg Yolk

et al. 1967

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“…This hypothesis is supported by studies of rat liver lipids after treatment of rats with tretinoin (all-f/wts-retinoic acid) revealing an increased hepatic synthesis of triglycer ides [46,47] carbon skeleton from mevalonic acid toward triglyceride synthesis instead of cholesterol [47]. Indeed, in rats a retinoid-induced decrease in hepatic cholesterol synthesis and hepatic cholesterol content has been report ed [48][49][50][51].…”

Section: Discussionmentioning

confidence: 86%

Characterization of Apoprotein Metabolism and Atherogenic Lipoproteins during Oral Isotretinoin Treatment

Melnik¹,

Bros²,

Plewig³

1987

Dermatology

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Apoprotein, lipoprotein and lipid parameters of 36 normolipidemic subjects (23 males, mean age 22.7 ± 7.6 years; 13 females, mean age 26.2 ± 9.8 years) receiving oral isotretinoin (mean daily dose 0.73 ± 0.26 mg/kg body weight) for nodulocystic acne (n = 18), severe acne papulopustulosa (n = 15), gram-negative folliculitis (n = 2) and papulopustular rosacea (n = l) were monitored before and during isotretinoin therapy at biweekly intervals over a period of 14.6 ± 5.6 weeks. Pretreatment values of mean plasma triglycerides increased significantly (p < 0.001) from 81.8 ± 31.9 mg/dl to 112.4 ± 38.7 mg/dl (47.4%) during isotretinoin treatment. With respect to the mean percent increase of plasma triglycerides from pretreatment levels, patients were classified as nonresponders ( < 10% triglyceride increase), responders ( > 10% < 50% triglyceride increase) and hyperresponders ( > 50% triglyceride increase), revealing a distribution of 25.0, 36.1 and 38.9%, respectively. Isotretinoin treatment had no influence on the isoelectric focusing pattern of apoprotein E isoforms and C apoproteins. In particular, apoprotein C-II, the cofactor of lipoprotein lipase, was not affected. No correlation between apoprotein E phenotypes (2/3, 3/3, 3/4) and the mean plasma triglyceride increase could be demonstrated. Apoprotein B-48, a marker of chylomicrons and atherogenic chylomicron remnants, could not be detected by SDS-PAGE. On the other hand in 21.0% of patients with preexisting mean lipoprotein Lp(a) levels of 18.1 ± 12.9 mg/dl a moderate increase of atherogenic Lp(a) to mean levels of 37.0 ± 22.0 mg/dl was observed. Pretreatment values of very-low-density lipoprotein (VLDL) apoprotein (apo) B (7.5 ± 2.0 mg/dl), low-density lipoprotein apo B (67.3 ± 17.5 mg/dl) and total plasma apo B (76.6 ± 19.0 mg/dl) increased significantly to levels of 10.3 ± 2.4 mg/dl (p < 0.001), 75.7 ± 15.8 mg/dl (p < 0.10) and 85.9 ± 17.7 mg/dl (p < 0.05), respectively. As lipoprotein lipase and hepatic lipase activities have been shown to be unaffected by isotretinoin treatment, our data support the hypothesis that isotretinoin induces hepatic oversecretion of VLDL, a condition resembling type IV hyperlipidemia in diabetics, familial hypertriglyceridemia or familial combined hyperlipidemia.

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“…In studies using chickens Wood (1960) demonstrated that vitamin A was the active hypocholesterolaemic factor in fish oils. Later, it was shown that vitamin A feeding prevented the rise in serum and liver cholesterol levels induced by dietary cholesterol in rats (Bring, Ricard & Zaehringer, 1965) and chickens (Wood & Topliff, 1961 ;Beeler, Rogler & Quackenbush, 1962;March & Biely, 1963). Sampson & Potter (1947) in a brief communication reported that vitamin A-deficient rats stored more cholesterol than controls when maintained on a diet containing cholesterol.…”

mentioning

confidence: 99%

Vitamin A status and the metabolism of cholesterol in the rat

Lakshmanan¹,

Phillips²,

Brien³

1969

Br J Nutr

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I . The interrelationship between cholesterol and vitamin A metabolism has been studied 2. The effect of cholesterol feeding in increasing the liver storage of cholesterol w-as 3. This effect was due to an increased rate of absorption of cholesterol and not due to a 4. Feeding of high levels of vitamin A markedly depressed the cholesterol absorption; in rats. enhanced during vitamin A deficiency. decreased turnover rate.however, its turnover was unaffected.

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Relationship between Cholesterol and Vitamin a Metabolism in Rats Fed at Different Levels of Vitamin A

Cited by 17 publications

References 16 publications

Effect of Dietary Vitamin A and Cholesterol on Cholesterol and Carotenoid Content of Plasma and Egg Yolk

Effect of Dietary Vitamin A and Cholesterol on Cholesterol and Carotenoid Content of Plasma and Egg Yolk

Characterization of Apoprotein Metabolism and Atherogenic Lipoproteins during Oral Isotretinoin Treatment

Vitamin A status and the metabolism of cholesterol in the rat

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