Vitamin dietary factors

Three hormones regulate turnover of calcium in the body (22). 1,25-Dihydroxycholecalciferol is a steroid derivative made by the combined action of the skin, Hver, and kidneys, or furnished by dietary factors with vitamin D activity. The apparent action of this compound is to promote the transcription of genes for proteins that faciUtate transport of calcium and phosphate ions through the plasma membrane. Parathormone (PTH) is a polypeptide hormone secreted by the parathyroid gland, in response to a fall in extracellular Ca(Il). It acts on bones and kidneys in concert with 1,25-dihydroxycholecalciferol to stimulate resorption of bone and reabsorption of calcium from the glomerular filtrate. Calcitonin, the third hormone, is a polypeptide secreted by the thyroid gland in response to a rise in blood Ca(Il) concentration. Its production leads to an increase in bone deposition, increased loss of calcium and phosphate in the urine, and inhibition of the synthesis of 1,25-dihydroxycholecalciferol. 

Other dietary factors implicated in prostate cancer include retinol, carotenoids, lycopene, and vitamin D consumption.5,6 Retinol, or vitamin A, intake, especially in men older than age 70, is correlated with an increased risk of prostate cancer, whereas intake of its precursor, [3-carotene, has a protective or neutral effect. Lycopene, obtained primarily from tomatoes, decreases the risk of prostate cancer in small cohort studies. The antioxidant vitamin E also may decrease the risk of prostate cancer. Men who developed prostate cancer in one cohort study had lower levels of l,25(OH)2-vitamin D than matched controls, although a prospective study did not support this.2 Clearly, dietary risk factors require further evaluation, but because fat and vitamins are modifiable risk factors, dietary intervention may be promising in prostate cancer prevention. 

The enzyme mediating remethylation, 5-methyltetrahy-drofolate-betaine methyltransferase (Fig. 40-4 reaction 4), utilizes methylcobalamin as a cofactor. The kinetics of the reaction favor remethylation. Faulty remethylation can occur secondary to (1) dietary factors, e.g. vitamin B12 deficiency (2) a congenital absence of the apoenzyme (3) a congenital inability to convert folate or B12 to the methylated, metabolically active form (see below) or (4) the presence of a metabolic inhibitor, e.g. an antifolate agent that is used in an antineoplastic regimen. 

The importance of dietary or endogenously synthesized vitamin D has long been recognized as a primary factor influencing the bioavailability of calcium. Some of the most exciting biochemical-nutritional research in recent years has been devoted to determining the mechanisms involved in vitamin D-calcium interactions. This research has been well reviewed in other publications. The objective of the symposium upon which this book is based was to review some of the other lesser-known dietary factors that appear to have an impact on the bioavailability of calcium. 

Chinn, H. I. 1981. Effects of Dietary Factors on Skeletal Integrity in Adults Calcium, Phosphorus, Vitamin D, and Protein. Life Sciences Research Office, Federation of American Societies for Experimental Biology, Bethesda, Md. 

Carnitine is present in nearly all organisms and in all animal tissues. The highest concentration is found in muscle where it accounts for almost 0.1% of the dry matter. Carnitine was first isolated from meat extracts in 1905 but the first clue to its biological action was obtained in 1948 when Fraenkel and associates described a new dietary factor required by the mealworm, Tenebrio molitor. At first designated vitamin Bt, it was identified in 1952 as carnitine. Most organisms synthesize their own carnitine from lysine side chains (Eq. 24-30). 

Another possible dietary factor concerns the essential fatty acid content of human and artificial milk. It has been postulated by Sinclair that many modern dietaries are deficient in the essential polyethenoid fatty acids (EFA) and that in consequence there is a rise in unesterified (and more active) vitamin D and in unesterified cholesterol. He has suggested that a part of the etiology of infantile idiopathic hypercalcemia may be attributed to EFA deficiency (S5). He has pointed to the lower content of certain unsaturated fatty acids in cow s milk as compared with human milk as a factor in the development of idiopathic hypercalcemia in artificially fed infants. He considers that dried milk has an even lower content of essential fatty acids than liquid cow s milk and that the longer it is stored the lower does the essential fatty acid content become. On the basis of some observations on rats, he suggests that a dietary deficiency of the essential fatty acids increases susceptibility to the possible toxic effects of vitamin D. The age of the rats, the duration of the essential fatty acid deficient diet, or the dosage of vitamin D is not mentioned, and there would appear to be no other experimental data to support these views. 

During the course of the symposium, several dietary factors that can influence xenobiotic metabolism were discussed in detail. Here we will attempt t summarize in the broadest terms how various classic nutrient groups might exert an influence on xenobiotic metabolism. For convenience, the dietary groups have been broken into carbohydrates, lipids, proteins, water-soluble vitamins, fat-soluble vitamins and trace elements. It is difficult to take any one group individually, and it must be kept in mind that the interactions are continuous and extremely complicated. 

The epidemiologic data, relative to dietary fiber, has been supported by animal studies but experiments with dietary fat have been conflicting and generally do not indicate a fat effect. Other dietary factors which associate with colon cancer in animal studies are deficits of lipotropes and of vitamin A. 

Measurement of blood tHcy is usually performed for one of three reasons (1) to screen for inborn errors of methionine metabolism (2) as an adjunctive test for cobalamin deficiency (3) to aid in the prediction of cardiovascular risk. Hyperhomocysteinemia, defined as an elevated level of tHcy in blood, can be caused by dietary factors such as a deficiency of B vitamins, genetic abnormalities of enzymes involved in homocysteine metabolism, or kidney disease. All of the major metabolic pathways involved in homocysteine metabolism (the methionine cycle, the transsulfuration pathway, and the folate cycle) are active in the kidney. It is not known, however, whether elevation of plasma tHcy in patients with kidney disease is caused by decreased elimination of homocysteine in the kidneys or by an effect of kidney disease on homocysteine metabolism in other tissues. Additional factors that also influence plasma levels of tHcy include diabetes, age, sex, lifestyle, and thyroid disease (Table 21-1). 

Vitamin B12 is an essential dietary factor, and a deficiency results in anemia and neurological damage. The vitamin assists two different enzymes in the production and the stabilization of methyl radicals. These methyl radicals are then used for the synthesis of important cellular components. 

Conversely, the addition of parathyroid hormone results in decreased 24-hydroxylation and increased 1-hydroxylation (Juan and DeLuca, 1977 Omdahl et al 2001 Wikvall, 2001). There is evidence that the high prevalence of vitamin D deficiency among people from the Indian subcontinent may he because of genetically determined high activity of calcidiol 24-hydroxylase, rather than cultural and dietary factors (Awumey et al., 1998). 

The term Vitamin E was introduced by Evans and Bishop to describe a dietary factor important for reproduction in rats [1]. Natural vitamin E includes two groups of closely related fat-soluble compounds, the tocopherols and tocotrienols, each with the four a-, y-,... 

Decarli A, Liati P, Negri E, Franceschi S, La Vecchia C. Vitamin A and other dietary factors in the etiology of esophageal cancer. Nutr Cancer 1987 10(l-2) 29-37. 

Perhaps it is more than happenstance that vitamin C is separated by name from the other water soluble B vitamins. Historically, this separation was the result of the normal procedure of labeling unknown dietary factors, as C was diflFerentiated from B— which later was shown to be a complex group rather than an individual, water-soluble vitamin. It was... 

CAS 62-49-7. (CH3)3N(OH)CH2CH2OH. Member of the vitamin B complex. Essential in the diet of rats, rabbits, chickens, and dogs. In humans it is required for lecithin formation and can replace methionine in the diet. There is no evidence of disease in humans caused by choline deficiency. It is a dietary factor important in furnishing free methyl groups for transmethylation has a lipotropic function. 

Precipitate Factor Elvehjem90 and coworkers found a dietary factor in liver, yeast, and milk, which they called the alcohol-ether precipitate factor. This factor can be adsorbed by activated carbon, but difficulty has been experienced in eluting the active substance. However, when carbon that contained the adsorbed factor was fed to vitamin-deficient animals, good growth was obtained. This suggests that elution In vitro could be accomplished under appropriate conditions. 

D-ribo-2,3,4,5-tetrahydroxypentyl)isoalloxazine and 7,8-dimethyl-10-ribityhsoalloxazine its formula is C17H20N4O6. Riboflavin has a molar mass of 376.37 grams (13.3 ounces). It is heat-stabile but easily degraded by light. Riboflavin was referred to as vitamin G in the early part of the twentieth century because it was recognized as a dietary factor needed for growth. Riboflavin was first isolated in 1879, and its chemical structure was determined in 1933. 

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