Vitamin gastric secretion

This condition has often been referred to in the past as juvenile pernicious anemia but it appears to be a quite separate entity. Confusion probably arose because there is a deficiency of intrinsic factor resulting in vitamin B12 malabsorption in both conditions. However, it differs from the disease in adults in that free acid is present in the gastric secretion (A8,L3,M5), the gastric mucosa is usually normal, and antibodies to intrinsic factor are not a feature. Megaloblastic anemia usually develops during the first 2 years of life but this depends on the amount of residual intrinsic factor available, and... 

Vitamin B] deficiency is commonly caused by pernicious anemia (PA). TA is an autoimmune disease resulting from the body s production of antibodies that recognize inlrinsic factor or other proteins of the parietal cell. The binding of antibodies to these proteins results in loss of their function. The parietal cells may be destroyed and be undetectable in patients with PA. The major defect in PA is gastric atrophy. 1 here may be a lack of all gastric secretions, including intrinsic factor, gastric acid, and pepsin. 

A large number of disorders are associated with cobalamin deficiency in infancy or childhood. Of these, the most commonly encountered is the Imerslund-Graesbeck syndrome, a condition that is characterized by inability to absorb vitamin B,2, with or without IF, and proteinuria. It appears to be due to an inability of intestinal mucosa to absorb the vitamin B,2 IF complex. The second most common of these is congenital deficiency of gastric secretion of IF. Very rarely, congenital deficiency of vitamin B12 in a breast-fed infant is due to deficiency of vitamin B12 in maternal breast milk as a result of unrecognized pernicious anemia in the mother. This is rare because most women with undiagnosed and untreated pernicious anemia are infertile. Additionally, there are some rare methylmalonic acidemias (acidurias) caused by inborn errors in homocysteine and methionine metabolism that are responsible for disorders in vitamin B status. ... 

Dietary fat depresses gastric secretion, slows gastric emptying and stimulates biliary and pancreatic flow, thereby facilitating the digestive process. Often, the acceptance of food and its palatability depends upon flavor and aroma. Although TAG in the pure state are relatively tasteless, they absorb and retain flavor of food. Furthermore, in combination with other nutrients, lipids provide a texture that enhances palatability and contributes to a feeling of satiety. Finally, dietary lipids serve as carriers for fat-soluble vitamins A, D, E, and K, and as an aid to then-absorption in the intestine. 

Gastric biopsy may exclude pernicious anemia if the fundus (corpus) mucosa is normal (Wood, 1951 Doig, 1954), but tests with radioactive vitamin B12 offer the best means of showing whether a patient has or has not a deficiency of intrinsic factor. If absorption is deficient it may be necessary to repeat the test after injecting carbachol to stimulate gastric secretion (Baker and Mollin, to be published). It is also necessary to show that a suitable dose of intrinsic factor restores Bn absorption to normal (see pages 158 to 160). 

A dietary substance, now known to be vitamin B-12, which was formerly thought to interact with the intrinsic factor of the gastric secretion to produce the antianemic factor. 

Ascorbate reacts with nitrite forming NO, NO2, and N2, so preventing the formation of nitrosa-mines. In addition to ascorbate in foods, there is considerable secretion of ascorbate in the gastric juice, and inhibition of gastric secretion for treatment of gastric ulcers, as well as reducing vitamin Bi2 absorption, also inhibits this presumably protective gastric secretion of ascorbate. 

Deficiency of vitamin Bj2 [cyanocobalamin (R = CN), or some other important cobalamins, e.g., adenosylcobalamin (R = adenosyl), hydroxocobal-amin (R = OH), methylcobalamin (R = CH3)], see Figures 7.1.1 and 7.1.3, causes a slow-developing disease, called pernicious anemia, in which the production of red blood cells is impaired. Absence of hydrochloric acid in gastric secretions (achlorhydria) is also characteristic of this condition. Without medical treatment, the disease will end in death in about 2 to 3 years. 

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. 

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... 

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. 

In general, ethanol in low to moderate amounts, is relatively benign to most body systems. A moderate amount of ethanol causes peripheral vasodilation, especially of cutaneous vessels, and stimulates the secretion of salivary and gastric fluids the latter action may aid digestion. On the other hand, ethanol consumption in high concentrations, as found in undiluted spirits, can induce hemorrhagic lesions in the duodenum, inhibit intestinal brush border enzymes, inhibit the uptake of amino acids, and limit the absorption of vitamins and minerals. In addition, ethanol can reduce blood testosterone levels, resulting in sexual dysfunction. 

Histamine, an important mediator of inflammation, gastric acid secretion and other allergic manifestations, contain an imidazole ring system. Thiamine, an essential vitamin, possesses a quaternized thiazole ring. 

Bi2 are only about 2 meg, it would take about 5 years for all of the stored vitamin B12 to be exhausted and for megaloblastic anemia to develop if Bi2 absorption were stopped. Vitamin B12 in physiologic amounts is absorbed only after it complexes with intrinsic factor, a glycoprotein secreted by the parietal cells of the gastric mucosa. Intrinsic factor combines with the vitamin Bi2 that is liberated from dietary sources in the stomach and duodenum, and the intrinsic factor-vitamin Bi2 complex is subsequently absorbed in the distal ileum by a highly selective receptor-mediated transport system. Vitamin Bi2 deficiency in humans most often results from malabsorption of vitamin B12 due either to lack of intrinsic factor or to loss or malfunction of the specific absorptive mechanism in the distal ileum. Nutritional deficiency is rare but may be seen in strict vegetarians after many years without meat, eggs, or dairy products. 

Pernicious anemia results from defective secretion of intrinsic factor by the gastric mucosal cells. Patients with pernicious anemia have gastric atrophy and fail to secrete intrinsic factor (as well as hydrochloric acid). The Schilling test shows diminished absorption of radioactively labeled vitamin B12, which is corrected when intrinsic factor is administered with radioactive B12, since the vitamin can then be normally absorbed. 

The story of vitamin B12 began with pernicious anemia, a disease that usually affects only persons of age 60 or more but which occasionally strikes children.3 Before 1926 the disease was incurable and usually fatal. Abnormally large, immature, and fragile red blood cells are produced but the total number of erythrocytes is much reduced from 4-6 x 106 mm-3 to 1- 3 x 106 mm-3. Within the bone marrow mitosis appears to be blocked and DNA synthesis is suppressed. The disease also affects other rapidly growing tissues such as the gastric mucous membranes (which stop secreting HC1) and nervous tissues. Demyelination of the central nervous system with loss of muscular coordination (ataxia) and psychotic symptoms is often observed. 

The imidazole ring occurs naturally in histamine 3.5, an important mediator of inflammation and gastric acid secretion. A quaternised thiazole ring is found in the essential vitamin thiamin 3.6. There are few naturally occurring oxazoles, apart from some secondary metabolites from plant and fungal sources. 

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