Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a placebo-controlled trial healthy volunteers and patients with hyperlipoproteinemias types II and IV received orally vitamin E at doses of 300 mg and 600 mg daily for 2 weeks. Serum tocopherol levels increased two-fold, but serum concentrations of total lipids, cholesterol, triglycerides, ceruloplasmin and transferrin remained unchanged. Dietary supplementation with vitamin E suppressed elevated concentrations of plasma lipid peroxides and this effect was correlated with an increase in serum antioxidant activity. In patients a mild platelet suppressant effect of vitamin E (600 mg daily) was observed. Feeding an atherogenic diet to rabbits for a week resulted in elevation of plasma lipid peroxides and a 90% decrease in arterial generation of prostacyclin. Enrichment of the atherogenic diet with 100 mg vitamin E daily prevented the increase in plasma lipid peroxides and protected the prostacyclin generating system in arteries. Thus, in hyperlipoproteinemias vitamin E corrects certain abnormalities of lipid metabolism which might predispose to atherosclerosis.
 ...
PMID:Dietary supplementation with vitamin E in hyperlipoproteinemias: effects on plasma lipid peroxides, antioxidant activity, prostacyclin generation and platelet aggregability. 390

To elucidate whether or not a vitamin E-deficient diet affects the rat aorta extracellular matrix, we examined the alterations in glycosaminoglycans (GAGs), as one of the components of the extracellular matrix of the aorta. The total amount of uronic acid, as an index of GAG, decreased significantly in the aorta of vitamin E-deficient rats. The components of GAG were identified as hyaluronic acid (HA), heparan sulfate (HS), dermatan sulfate (DS) and chondroitin sulfate (CS) by electrophoresis together with enzymic digestion. The amount of sulfated GAGs, especially the amount of DS and CS, decreased in the aorta of vitamin E-deficient rats. The biosynthetic activity of GAG was determined by using [3H]glucosamine and [35S]sulfate. The total biosynthetic activity of GAG and the incorporation of [3H]glucosamine into HA, HS, DS and CS decreased markedly in the aorta of vitamin E-deficient rats. The decrease in the production of sulfated GAGs, especially DS, which is involved in the potent antithrombogenic activity, could be related to the lower anticoagulant activity in the aorta of vitamin E-deficient rats.
Atherosclerosis 1985 Apr
PMID:Alterations in glycosaminoglycans of the aorta of vitamin E-deficient rats. 392 63

The biochemical, clinical, and genetic features were examined in the proband (homozygote) and heterozygotes (n = 17) affected with familial apolipoprotein A-I and C-III deficiency, variant II (previously described as apolipoprotein A-I absence). The proband was a 45-year-old white female with mild corneal opacification and significant three-vessel coronary artery disease (CAD), who died shortly after bypass surgery. Autopsy findings included significant atherosclerosis in the coronary and pulmonary arteries and the abdominal aorta as well as extracellular stromal lipid deposition in the cornea. No reticuloendothelial lipid deposits in the liver, bone marrow, or spleen were noted (unlike Tangier disease). Laboratory features included marked high density lipoprotein (HDL) deficiency and undetectable plasma apolipoproteins (apo) A-I and C-III. The percentage of plasma cholesterol in the unesterified form was normal at 30%. The activity and mass of lecithin:cholesterol acyltransferase (LCAT) were 42% and 36% of normal, respectively, and the cholesterol esterification rate was 43% of normal. Deficiencies of plasma vitamin E and essential fatty acid (linoleic, C18:2) were also noted. Evaluation of plasma lipoproteins and apolipoproteins in 37 kindred members revealed 17 heterozygotes with HDL cholesterol values below the 10th percentile of normal. Of these, all had apoA-I levels more than one standard deviation below the normal mean, and 37.5% had a similar decrease in apoC-III values. Mean (+/- SD) plasma HDL cholesterol, apoA-I, and apoC-III values (mg/dl) in heterozygotes were 54.0%, 62.4%, and 79.2% of normal, respectively. No evidence of CAD was observed in 10 heterozygotes 40 years of age or less; however, CAD was detected in 3 of 7 heterozygotes over 40 years of age, one of whom died at age 56 years of complications of myocardial infarction and stroke. The inheritance pattern in this kindred was autosomal codominant. ApoA-I isolated from a heterozygote had an isoelectric focusing pattern and amino acid composition similar to normal. Utilizing DNA isolated from two obligate heterozygotes, no abnormalities in the apoA-I or apoC-III genes were detected by Southern blot analysis utilizing specific probes following restriction enzyme digestion. The data indicate that familial apolipoprotein A-I and C-III deficiency, variant II, is similar to variant I (described by Norum et al. 1982. N. Engl. J. Med. 306: 1513-1519), but differs at the clinical level (lack of xanthomas), the biochemical level (lack of detectable apoA-I, lower apoA-II level), and at the gene level.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Familial apolipoprotein A-I and C-III deficiency, variant II. 393 6

This paper discusses the nutritional requirements for fat in infants and children in the light of the dietary alterations recently proposed by the Inter-Society Commission on Heart Disease Resources. It is not well known what the requirement for total fat and for serum cholesterol level during the first year of life should be. It is known that the only proved requirement for fat is linoleic acid, and that a logical fat intake would be that supplied by breast milk. 80% of American infants are fed with formulas which are not supplemented with the essential vitamin E. After infancy fat requirements change, and body stores are sufficient to insure against fatty acid deficiency. The dietary intake of American children is high in quantities of saturated fats and cholesterol, possibly leading to atherosclerosis later in life. The question is whether this cholesterogenic diet is harmful to all Americans or to a limited number of clinically discernible subjects, i.e., those children genetically predisposed to hyperlipoproteinimia. Such predisposition could be diagnosed at birth by screening of the umbilical cord blood, and checked again at school age and at adolescence. Thus, although limitation of a cholesterogenic diet to prevent obesity is reasonable, restricting cholestrogenic foods in everyone for the unproved distant goal of reducing atherosclerosis is dubious.
 ...
PMID:Fat nutrition and diet in childhood. 463 20

The most commonly known function of vitamin E in vivo is the prevention of undue oxidation of polyunsaturated fatty acids. It has been claimed that in vitamin E deficiency, the arachindonic content of the tissue increases as does the content of higher unsaturated fatty acid. In experimental chronic ozone intoxication, vitamin E was shown to protect against ozone poisoning. There was no evidence however that a rapid turnover of fatty acids occurred during ozone exposure. A possibility is that the increased tissue content of higher polyunsaturated fatty acids is due to the arrest of their further metabolization through lack of vitamin E. The higher polyunsaturated fatty acids are synthesized from linoleic and linolenic acids; in turn, the unsaturated fatty acids with 3 or more double bonds are the basic compounds of prostaglandins. Important functions of prostaglandins include: prevention of blood platelet aggregation; blood vessel dilatation; lowering of blood pressure; stimulation of smooth muscle; and inhibition of fat mobilization by noradrenaline. Diminished activity of one or more of the prostaglandins may be a promoting factor for atherosclerosis and its complication, especially myocardial infarction. These diseases may be prevented by increasing daily consumption of polyunsaturated fatty acids, mainly linoleic acid which can be derived from vegetable oils.
 ...
PMID:Ozone, vitamin E, fatty acids, prostaglandins, atherosclerosis and its complications. 470 14

There are two families of essential fatty acids, the linoleic and linolenic. Linoleic acid (C18:2n-6), found mainly in vegetable seed oils, is desaturated and elongated in the body, forming arachidonic acid (C20:4n-6). Linolenic acid (C18:3n-3), the main dietary source of which is leaves, is desaturated and elongated, forming two fatty acids that are prevalent in fish oils: timnodonic (C20:5n-3) and clupanodonic (C22:6n-3). EFA are very easily peroxidized in air, but vitamin E protects against this. There are three functions of EFA. The most important is as part of phospholipids in all animal cellular membranes: in deficiency of EFA faulty membranes are formed. A second is in the transport and oxidation of cholesterol: EFA tend to lower plasma cholesterol. A third function is as precursors of prostanoids which are only formed from EFA. Deficiency of EFA in experimental animals causes lesions mainly attributable to faulty cellular membranes: sudden failure of growth, lesions of skin and kidney and connective tissue, erythrocyte fragility, impaired fertility, uncoupling of oxidation and phosphorylation. In man pure deficiency of EFA has been studied particularly in persons fed intravenously. A relative deficiency (that is, a low ratio in the body of EFA to long-chain saturated fatty acids and isomers of EFA) is common on Western diets and plays an important part in the causation of atherosclerosis, coronary thrombosis, multiple sclerosis, the triopathy of diabetes mellitus, hypertension and certain forms of malignant disease. Various factors affect the dietary requirement of EFA.
 ...
PMID:Essential fatty acids in perspective. 646 3

The composition of vitamin E in serum and lipoproteins was determined in type I, IIa, IIb, IV and IV hyperlipoproteinemia and in normal subjects. Vitamin E was not specifically associated with any one of the lipoproteins but increased vitamin E levels were observed in VLDL when triacylglycerols level was increased (types IIb and IV); the same observations were noted in LDL when cholesterol level was increased (type IIa).
Atherosclerosis 1984 Dec
PMID:Vitamin E and lipoproteins in hyperlipoproteinemia. 652 49

A significant increase in high-density lipoprotein-cholesterol after the ingestion of short-term megadoses of vitamin E has been documented in the recent literature. No attempt has been made to examine the effect of vitamin E supplementation on the serum lipids in chronic renal patients undergoing maintenance hemodialysis. This patient group typically exhibits subnormal high-density lipoprotein-cholesterol levels which may be a factor responsible for their increased mortality rate from atherosclerosis. In the present study, seven male renal patients on dialysis were given 600 IU of vitamin E daily for 4 wk. The level of total, free, and esterified cholesterol and triglyceride in whole serum and high-density lipoprotein were measured pre- and postregimen. No significant change was noted in any of the parameters examined for the group as a whole. Our results suggest that short-term high-dose vitamin E ingestion is unlikely to benefit the majority of renal patients on maintenance hemodialysis in regards to their circulating levels of high-density lipoprotein-cholesterol.
 ...
PMID:Effect of vitamin E supplementation on serum and high-density lipoprotein-cholesterol in renal patients on maintenance hemodialysis. 688 Oct 82

Three experiments were conducted with adult, male Japanese quail (Coturnix coturnix japonica) from 5 through 14 weeks of age. In Experiment 1, quail fed a cholesterol-free diet were compared with quail fed .5% of United States Pharmacopoeias (USP), recrystallized (RCR), or oxidized (OXI) cholesterol preparations. In Experiment 2, .5% OXI cholesterol was fed alone and with .1% butylated hydroxytoluene (BHT) or 100 mg d-alpha-tocopherol acetate/kg of diet and compared with .5% RCR cholesterol. Experiment 3 was the same as Experiment 2 except the BHT treatment was deleted. In comparison to RCR-treated quail, OXI-treated quail exhibited significantly increased serum (P less than .05) and liver (P less than .01) cholesterol concentrations and increased severity of atherosclerotic lesions (P less than .05). Addition of vitamin E to the OXI cholesterol diet appeared to reduce severity of atherosclerotic lesions. Vitamin E did not completely prevent atherosclerosis nor did it change the proportion of the quail population that exhibited lesions.
 ...
PMID:Atherosclerosis in cholesterol-fed Japanese quail: evidence for amelioration by dietary vitamin E. 717 1

The FAO/WHO Rome Report recommended an increase in the consumption of fat in countries where malnutrition is endemic; for maintenance, 3% of the dietary energy as essential fatty acids (EFA) may be adequate; in pregnancy and lactation an additional 1.5 to 2.4% energy as EFA is needed. For population at high risk for atherosclerosis and coronary heart disease (CHD) the recommendations were to decrease saturated fat in particular and increase EFA intake in the diet, reduce sugar, alcohol and cholesterol. These recommendations were similar to those of the Royal College of Physicians but the report went further by saying that EFA loss through industrial hydrogenation should be minimized and associated nutrients such as vitamin E and carotene should be restored if lost in processing. In terms of production, they asked for an increase in edible plant oils in developing countries and requested that intensive animal feeding and breeding should be corrected to avoid the excess accumulation of saturated fats. In addition, the Rome Report requested meaningful labelling of amounts and quality of fat in foods containing added fats. The basic aims of the Report were to state the position of lipid nutrition. The issue of the nutrient correction in terms of CHD cannot properly be discussed without taking into account the essential components which are needed for the integrity and development of the vascular system.
 ...
PMID:The role of essential fatty acids and prostaglandins. 746 59


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>