The Effect of Tocopherol on High-density Lipoprotein Cholesterol: A Clinical Observation

Hermann, William J.; Ward, Karen; Faucett, James

doi:10.1093/ajcp/72.5.848

Cited by 60 publications

(20 citation statements)

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“…Hermann et al (30) supplemented human subjects with 600 IU of = -tocopherol for 30 days; an increase in HDLcholesterol and no change in triglycerides or total cholesterol occurred. These results were not confirmed by other investigators who used the same experimental protocol (31,32).…”

Section: Resultsmentioning

confidence: 99%

Influences of alpha-tocopherol on cholesterol metabolism and fatty streak development in apolipoprotein E-deficient mice fed an atherogenic diet

Peluzio

Homem

César

et al. 2001

Braz J Med Biol Res

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Although the role of oxidized lipoproteins is well known in atherogenesis, the role of vitamin E supplementation is still controversial. There is also little information about cholesterol metabolism (hepatic concentration and fecal excretion) in the new models of atherosclerosis. In the present study, we evaluated the effect of moderate vitamin E supplementation on cholesterol metabolism and atherogenesis in apolipoprotein E (apo E)-deficient mice. Apo E-deficient mice were fed an atherogenic diet containing 40 or 400 mg/kg of = -tocopherol acetate for 6 weeks. Total cholesterol in serum and liver and 3-OH-=-sterols in feces, and fecal excretion of bile acids were determined and histological analyses of aortic lesion were performed. A vitamin Erich diet did not affect body weight, food intake or serum cholesterol. Serum and hepatic concentrations of cholesterol as well as sterol concentration in feces were similar in both groups. However, when compared to controls, the = -tocopherol-treated mice showed a reduction of about 60% in the atherosclerotic lesions when both the sum of lesion areas and the average of the largest lesion area were considered. These results demonstrate that supplementation of moderate doses of = -tocopherol was able to slow atherogenesis in apo E-deficient mice and to reduce atherogenic lipoproteins without modifying the hepatic pool or fecal excretion of cholesterol and bile acids.

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Section: Resultsmentioning

confidence: 99%

Influences of alpha-tocopherol on cholesterol metabolism and fatty streak development in apolipoprotein E-deficient mice fed an atherogenic diet

Peluzio

Homem

César

et al. 2001

Braz J Med Biol Res

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“…Whether HDL cholesterol concentrations change in humans taking vitamin E supplements remains a controversial topic. Since the late 1970s, vitamin E supplements have been found to increase ( 86,87 ), decrease ( 88 ), or leave unchanged ( 89 ) the circulating HDLcholesterol concentrations. The differences in these outcomes may have to do with the various HDL regulators, as discussed below.…”

Section: Lipoprotein Transportmentioning

confidence: 99%

Mechanisms for the prevention of vitamin E excess

Traber

2013

Journal of Lipid Research

117

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“…However, several workers showed that vitamin E may slow the progress of atherosclerosis by modifying the synthesis and degradation of lipids in the arterial wall 26 and/or by increasing the proportion of blood cholesterol in the electrophoretic HDL-C fraction. 21 The view that vitamin C supplementation into rats for five weeks or more could affect the concentration of plasma concentrations is further supported by the work of Riemersma and co-workers 16 who showed that low plasma concentrations of vitamin C were related to an increased risk of angina pectoris in men. In addition, they reported that vitamin C levels are lower in cigarette smokers than in nonsmokers.…”

Section: Discussionmentioning

confidence: 97%

“…This result is also in agreement with results reported elsewhere. [21][22][23][24] In 1982, Haeger 25 suggested that when vitamin E is maintained in excess of that provided by a normal diet in humans, it is beneficial in intermittent claudication and perhaps other manifestations of atherosclerosis. However, several workers showed that vitamin E may slow the progress of atherosclerosis by modifying the synthesis and degradation of lipids in the arterial wall 26 and/or by increasing the proportion of blood cholesterol in the electrophoretic HDL-C fraction.…”

Section: Discussionmentioning

confidence: 99%

Effect of Vitamins C and E Intake on Plasma Lipid Concentrations in Rats

Khoja

Marzouki

1994

Annals of Saudi Medicine

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Changes in the plasma lipid levels were investigated among rats fed an atherosclerotic-promoting diet containing 0.5% cholesterol and rats fed the same diet with added vitamin C (ascorbic acid), vitamin E (a-tocopherol) and vitamins C + E from one to seven weeks. Total cholesterol (TC) and triglycerides (TG) were significantly increased in rats fed a hyperlipidemic diet from the third week to the seventh week, whereas high density lipoprotein cholesterol (HDL-C) was not affected. Rats supplemented with 5 mg vitamin C, 5 mg vitamin E or 5 mg vitamin C + 5 mg vitamin E per day for four to seven weeks showed significant decrease in the concentration of TC and TG. HDL-C was only affected at the seventh week with vitamin C alone, whereas it was significantly increased with vitamin E alone and vitamins C + E at five to seven weeks. However, supplementation of vitamins C, E or C + E for less than four weeks has no significant effect on plasma lipid concentrations. The antioxidant effect of vitamins C and E is probably a time-dependent process that significantly lowers plasma lipids between week four and week seven following administration of these vitamins. It is therefore suggested that the incidence of coronary heart disease (CHD) may be reduced in lowering plasma lipid levels by dietary supplementation of vitamins C or E. Ann Saudi Med 1994;14(5):371-374. SM Khoja, ZMH Marzouki, Effect of Vitamins C and E Intake on Plasma Lipid Concentrations in Rats. 1994; 14(5): 371-374Coronary heart disease (CHD) is one of the major causes of morbidity and mortality. A positive correlation has been demonstrated between raised serum lipids and the incidence of CHD and atherosclerosis in humans. Cholesterol is the lipid most frequently implicated in this relationship. The cholesterol-rich low density lipoprotein (LDL) has met all criteria of a primary risk factor for CHD. However, the levels of the various lipoproteins and their apolipoproteins have been found to be altered in patients with CHD. Recent research in the pathophysiology of atherosclerosis focused on modifications of lipoproteins increasing their atherogenic potential.1 Those cells that are responsible for the formation of atherosclerotic lesions, namely the macrophages, are normally not able to take up LDL in considerable amounts. Only after having modified LDL by acetylation, Goldstein and Brown succeeded in loading macrophages with LDL.2 This process leads to the formation of so-called lipid laden foam cells. The Σ-amino groups of the lysine residues on apolipoprotein B (Apo B) become blocked by acetylation and the net negative charge of the lipoprotein is strongly enhanced. Looking for other physiological mechanisms of LDL modification, Henriksen et al. 3 observed that macrophages, previously incubated with cultured endothelial cells, demonstrate enhanced degradation of LDL and storage of cholesterol esters. In following reports, it was shown that lipid peroxidation is involved in this modification of LDL by cultured cells. For reviews see references 4 to 6.Recent ...

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The Effect of Tocopherol on High-density Lipoprotein Cholesterol: A Clinical Observation

Cited by 60 publications

References 0 publications

Influences of alpha-tocopherol on cholesterol metabolism and fatty streak development in apolipoprotein E-deficient mice fed an atherogenic diet

Influences of alpha-tocopherol on cholesterol metabolism and fatty streak development in apolipoprotein E-deficient mice fed an atherogenic diet

Mechanisms for the prevention of vitamin E excess

Effect of Vitamins C and E Intake on Plasma Lipid Concentrations in Rats

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