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PubMed2000

ALCOHOL: its metabolism and interaction with nutrients.

In the past, alcoholic liver disease was attributed exclusively to dietary deficiencies, but experimental and judicious clinical studies have now established alcohol's hepatotoxicity. Despite an adequate diet, it can contribute to the entire spectrum of liver diseases, mainly by generating oxidative stress through its microsomal metabolism via cytochrome P4502E1 (CYP2E1). It also interferes with nutrient activation, resulting in changes in nutritional requirements. This is exemplified by methionine, one of the essential amino acids for humans, which needs to be activated to S-adenosylmethionine (SAMe), a process impaired by liver disease. Thus, SAMe rather than methionine is the compound that must be supplemented in the presence of significant liver disease. In baboons, SAMe attenuated mitochondrial lesions and replenished glutathione; it also significantly reduced mortality in patients with Child A or B cirrhosis. Similarly, decreased phosphatidylethanolamine methyltransferase activity is associated with alcoholic liver disease, resulting in phosphatidylcholine depletion and serious consequences for the integrity of membranes. This can be offset by polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated phosphatidylcholines comprising dilinoleoylphosphatidylcholine (DLPC), which has high bioavailability. PPC (and DLPC) opposes major toxic effects of alcohol, with down-regulation of CYP2E1 and reduction of oxidative stress, deactivation of hepatic stellate cells, and increased collagenase activity, which in baboons, results in prevention of ethanol-induced septal fibrosis and cirrhosis. Corresponding clinical trials are ongoing.

Alcohol Dehydrogenase↗
PubMed2000

The role of the microsomal triglygeride transfer protein in abetalipoproteinemia.

The microsomal triglyceride transfer protein (MTP) is a dimeric lipid transfer protein consisting of protein disulfide isomerase and a unique 97-kDa subunit. In vitro, MTP accelerates the transport of triglyceride, cholesteryl ester, and phospholipid between membranes. It was recently demonstrated that abetalipoproteinemia, a hereditary disease characterized as an inability to produce chylomicrons and very low-density lipoproteins in the intestine and liver, respectively, results from mutations in the gene encoding the 97-kDa subunit of the microsomal triglyceride transfer protein. Downstream effects resulting from this defect include malnutrition, very low plasma cholesterol and triglyceride levels, altered lipid and protein compositions of membranes and lipoprotein particles, and vitamin deficiencies. Unless treated, abetalipoproteinemic subjects develop gastrointestinal, neurological, ophthalmological, and hematological abnormalities.

Abetalipoproteinemia↗
PubMed1985

Vitamin levels in chronic renal failure and need for supplementation.

Deficiencies of water-soluble vitamins may occur in uremic patients mainly because of restricted consumption and of loss during chronic hemo- and peritoneal dialysis. Although the daily requirement for most vitamins is not well defined in chronic renal failure supplementation of the vitamins thiamine, riboflavin, pyridoxine, pantothenic acid, niacin and ascorbic acid, the form of one multivitamin preparation without vitamin A as well as folic acid in dialysis patients after each dialysis is recommended. There is no need for vitamin B12, vitamin A and vitamin E.

Ascorbic Acid↗
PubMed1986

[Evaluation of dietary vitamin intake in Burgundy (France)].

The daily intake of vitamin B1, B2, B6, PP, C, A, D and E was investigated in 297 adult subjects, undergoing a check-up examination in a Health Center in Burgundy, by the 7-day self-recorded prospective protocol, to determine the prevalence of vitamin deficiency risks in an area of a West European Country. The daily vitamin intake was lower than the French Recommended Dietary Allowances: RDA (CNERNA, 1981). The intake was between 50 and 80% of RDA for vitamin B1 in 58%, B2 in 24%, B6 in 59%, PP in 43%, C in 21%, A in 8%, D in 0.6%, E in 53% of the female population and for B1 in 40%, B2 in 18.5%, B6 in 59%, PP in 46%, C in 27%, A in 11%, D in 7% and E in 47% of the male population. The daily vitamin intake was less than half of RDA vor vitamin B1 in 11%, B2 in 0.6%, B6 in 33%, PP in 6.3%, C in 4.5%, A in 0.6%, D in 98%, E in 36% in the females and for B1 in 3%, B6 in 8.5%, PP in 3.5%, C in 5%, A in 0.7%, D in 91% and E in 9% in the males. The use of a probability analysis for estimating vitamin deficiencies showed intakes below their own requirement in 37.8% for B1, 18% for B2, 58.6% for B6, 46% for PP, 29% for C, 8.3% for A, 98% for D and 43.4% for E in the males and 62.5% for B1, 20.9% for B2, 86% for B6, 46% for PP, 24% for C, 9.2% for A, 98% for D and 59.7% for E in the females. Significant correlations were found between the daily vitamin intake and the caloric intake for B1 (r = 0.64), B2 (r = 0.46), B6 (r = 0.64) and PP (r = 0.62). The significantly lower caloric intake in females than in males explains a higher proportion of vitamin deficiencies for B1, B2, B6 and PP in this population. The consumption of green vegetables and fresh fruit, and, consequently, vitamin C intake, was higher in females. Although it was not possible to determine to what extent the vitamin intake deficiency contributes to an impaired biochemical vitamin status, the dietary data of this study supply sufficient information to demonstrate high prevalences of deficient vitamin status in France, particularly for B1, B6 and E.

Adult↗