Gastric vitamin

A2. Allen, R. H., and Mehlman, C. S., Isolation of gastric vitamin B12 binding proteins using affinity chromatography. I. Purification and properties of human intrinsic factor. /. Biol. Chem. 248, 3660-3669 (1973). 

Clinical manifestation of vitamin B 2 deficiency is usually a result of absence of the gastric absorptive (intrinsic) factor. Dietary deficiency of vitamin B 2 is uncommon and may take 20 to 30 years to develop, even in healthy adults who foUow a strict vegetarian regimen. An effective enterohepatic recycling of the vitamin plus small amounts from bacterial sources and other contaminants greatly minimizes the risk of a complete dietary deficiency. Individuals who have a defect in vitamin B 2 absorption, however, may develop a deficiency within three to seven years. 

Dietary deficiency in the absence of absorption defects can be effectively reversed with oral supplementation of 1 p.m of vitamin B 2 daily. If deficiency is related to a defect in vitamin absorption, daily doses of 1 pg adininistered subcutaneously or intramuscularly are effective (33). However, a single intramuscular dose of 100 pg of cobalamin once per month is adequate in patients with chronic gastric or ileal damage. Larger doses are generally rapidly cleared from the plasma into the urine and are not effective unless the patient demonstrates poor vitamin retention. 

In more recent times, large doses of vitamin C have been claimed to prevent the common cold, cure infertility, delay the onset of symptoms in acquired immunodeficiency syndrome (AIDS), and inhibit the development of gastric and cervical cancers. None of these claims have been backed by medical evidence, however. In the largest study yet done of the effect of vitamin C on the common cojd, a meta-analysis of more than 100 separate trials covering 40,000 people found no difference in the incidence of colds between those who took supplemental vitamin G regularly and those who did not. When taken during a cold, however, vitamin C does appear to decrease the cold s duration by 8%. 

Also, the outcome covers a large spectrum. Autoantibodies can specifically block an important protein (such as the gastric intrinsic factor required for the uptake of orally taken vitamin B12), or the receptor for —> acetylcholine (as in myasthenia gravis), but also can... 

The treatment of an autoimmune disease very much depends on the nature of the clinical outcome it causes. Although the formation of autoantibodies causes the inactivation of the gastric intrinsic factor, the subsequent shortage of vitamin B12 can be easily overcome by supplying it via an parenteral route. Lifelong immunosuppression (with all its side effects) thus is inappropriate. When, however, as in sympathetic ophtalmia, after damage of the first eye the second eye is endangered, an even drastic immunosuppression is mandatory. 

Vitamin B12 is special in as far as its absorption depends on the availability of several secretory proteins, the most important being the so-called intrinsic factor (IF). IF is produced by the parietal cells of the fundic mucosa in man and is secreted simultaneously with HC1. In the small intestine, vitamin B12 (extrinsic factor) binds to the alkali-stable gastric glycoprotein IF. The molecules form a complex that resists intestinal proteolysis. In the ileum, the IF-vitamin B 12-complex attaches to specific mucosal receptors of the microvilli as soon as the chymus reaches a neutral pH. Then either cobalamin alone or the complex as a whole enters the mucosal cell. 

Isoniazid Take this drug 1 hour before or 2 hours after meals. However, if gastric upset occurs, take isoniazid with food. Notify the primary health care provider of weakness, yellowing of the skin, loss of appetite, darkening of the urine, skin rashes, or numbness or tingling of the hands or feet. Avoid tyrainine-containing foods (see Chap. 31). To prevent pyridoxine (vitamin Bg) deficiency, 6 to 50 mg of pyridoxine daily may be prescribed. 

Pernicious anemia Anemia resulting from lack of secretions by the gastric mucosa of the intrinsic fador essential to the formation of RBCS and the absorption of vitamin B ... 

Megaloblastic anemias Deficiency of vitamin 6,2 Decreased absorption of 6,2, often due to a deficiency of intrinsic factor, normally secreted by gastric parietal cells... 

Mirvish (53,54) discovered that vitamin C could inhibit ni-trosation reactions. The purely chemical interaction of ascorbic acid with nitrite has been studied for theoretical reasons and because of its importance in the preservation of foods. This interaction has received increased attention for minimizing the presence of nitrosamines and nitrosamides in the environment, and especially in foods. We have studied the relationship in gastric carcinogenesis between high levels of nitrite, including pickling, and of vitamin C as a protective and inhibiting element. 

Botterweck, A. A. et al., Vitamins, carotenoids, dietary fiber, and the risk of gastric carcinoma results from a prospective study after 6.3 years of foUow-up, Cancer, 88, 131, 2000. 

Armario, A., Campmany, L., Borras, M. and Hidalgo, J. (1990). Vitamin E-supplemented diets reduce lipid peroxidation but do not alter either pituitary-adrenal, glucose, and lactate responses to immobilization stress or gastric ulceration. Free Rad. Res. Commun. 9, 113-118. 

In the stomach, carotenoids are exposed to acid environments. This can lead to carotenoid isomerization, which can change carotenoid antioxidant properties, solubility, and absorption. In humans, (3-carotene absorption is reduced when the pH of the gastric fluids is below 4.5 (Tang and others 1995). Vitamin E consumption seems to reduce carotenoid absorption in animals, presumably because vitamin E and carotenoids compete for absorption (Furr and Clark 1997). Dietary sterols, such as those in sterol-supplemented functional foods, are also known to decrease carotenoid absorption. 

Vitamin B12- and folate-deficiency anemias are characterized by pallor, icterus, and gastric mucosal atrophy. Vitamin B12 anemia is distinguished by neuropsychiatric abnormalities (e.g., numbness, paresthesias, irritability), which are absent in patients with folate-deficiency anemia. 

There are several steps in the absorption of vitamin B. In the stomach and lumen of the small intestine it is hydrolysed from its (peptide) links with the proteins of which it is a component. It then attaches to gastric intrinsic factor, which is a glycoprotein of molecular mass about 50 000 kDa, to form a complex. This protects the vitamin from being damaged by acid in the stomach. The complex is carried into the ileum, where it binds to a receptor on the surface of the absorptive cells and is released from the intrinsic factor within the absorptive cell, hi the portal venous blood, it is transported to the liver bound to the vitamin B 12-binding protein, which also protects the vitamin. 

Cobalamine can only be resorbed in the small intestine when the gastric mucosa secretes what is known as intrinsic factor—a glycoprotein that binds cobalamine (the extrinsic factor) and thereby protects it from degradation. In the blood, the vitamin is bound to a special protein known as trans-cobalamin. The liver is able to store vitamin Bi2 in amounts suf cient to last for several months. Vitamin B12 deficiency is usually due to an absence of intrinsic factor and the resulting resorption disturbance. This leads to a disturbance in blood formation known as pernicious anemia. 

Retief, F. P., Gottlieb, C. W., Kochwa, S., Pratt, P. W., and Herbert, V., Separation of vitamin Birbinding proteins of serum, gastric juice and saliva by rapid DEAE cellulose chromatography. Blood 29, 501-516 (1967). 

Various factors are required for regular fat digestion. Sublingual lipase and eventually a gastric lipase — which are both stable in an acidic environment — start digesting dietary fats in the stomach. In the intestine, pancreatic bicarbonate as well as bile acids are essential for emulsification of fats and fat-soluble substances which are then cleaved by pancreatic lipases. The cleavage products are incorporated into micelles and can then penetrate the unstirred water layer (UWL) which covers the intestinal surface. There, they can deliver the cleavage products of dietary fats as well as fat-soluble substances (e.g., carotenoids, vitamin E, vitamin A) to the luminal surface of the enterocytes. 

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