Absorption, dietary

The mucosal cells of the proximal small bowel regulate iron absorption. Dietary and administered iron is actively transported into the gut mucosal cell, probably involving a protein DMTl though the precise details have not been established. Two other proteins, hephaestin and ferroportin 1, appear to be involved in intracellular transport and release into the plasma respectively. Regulation of absorption may involve one or more of (1) control of mucosal uptake (2) retention of iron in storage form in the mucosal cell and (3) transfer from the mucosal cell to the plasma. Increased erythropoietic activity also stimulates increased absorption. Iron that is not needed by the body may be bound to a protein (apoferritin) as ferritin and lost into the gut lumen when the mucosal cell is shed (2-3 days). Iron is eUminated at a near constant rate in the faeces of healthy people. 

Vitamin absorption. Dietary fat serves as a carrier of the lipid-soluble vitamins. All are transported into cells of the small intestine in association with fat molecules. Therefore a diet that is too low in fat can result in a deficiency of these four vitamins. 

Fat constitutes approximately 38% of the calories in the average North American diet. Of this, more than 95% of the calories are present as triacylglycerols (3 fatty acids esterified to a glycerol backbone). During ingestion and absorption, dietary triacylglycerols are broken down into their constituents and then reassembled for transport to adipose tissue in chylomicrons (see Chapter 2). Thus, the fatty acid composition of adipose triacylglycerols varies with the type of food consumed. 

Atovaquone is a highly lipophilic compound, which shows considerable inter-individual variability in absorption. Dietary fat increases the rate and extent of atovaquone absorption from both the suspension and the tablets, probably by increasing its solubility in the gut. The suspension has about a twofold higher oral bioavailability than the tablets when given with food or when fasting. 

Certain ions, e.g., oxalate and phosphate, can bind Ca within the intestinal canal and high intake of phosphate can restrict calcium absorption. A similar effect is encountered by phytic acid (inositol hexaphosphate) that is present in high amounts in certain cereals. Disturbances in the fat absorption (dietary) decreases the calcium absorption because Ca is bound to nonabsorbable fatty acids. 

Calcium Adequate calcium intake is required to maintain bone mineral density and reduce the risk of osteoporosis in the elderly. In addition to the reduced absorption of calcium by elderly people that results from age-related changes in vitamin D metabolism, the elderly also show a reduced ability to increase the efficiency of calcium absorption as an adaptive response to low-calcium diets. Also, as noted earlier, the low-acid conditions resulting from atrophic gastritis can reduce calcium absorption. Dietary calcium reacts with hydrochloric acid in the stomach to form soluble calcium chloride, which is absorbed in the small intestine. In the United States, the recommended calcium intake is 1200mg/day for men and women older than age 70. Many elderly people may benefit from calcium supplements. 

The amount of each element required in daily dietary intake varies with the individual bioavailabihty of the mineral nutrient. BioavailabiUty depends both on body need as deterrnined by absorption and excretion patterns of the element and by general solubiUty, and on the absence of substances that may cause formation of iasoluble products, eg, calcium phosphate, Ca2(P0 2- some cases, additional requirements exist either for transport of substances or for uptake or binding. For example, calcium-binding proteias are iavolved ia calcium transport an intrinsic factor is needed for vitamin cobalt,... 

One method of treatment is to inject calcitonin, which decreases blood Ca " concentration and increases bone calcification (33). Another is to increase the release of calcitonin into the blood by increasing the blood level of Ca " ( 4). This latter treatment is accompHshed by increasing Ca " absorption from the intestine requiring dietary calcium supplements and avoidance of high phosphate diets. The latter decrease Ca " absorption by precipitation of the insoluble calcium phosphate. 

Proteins and Meals. Nutritional properties of the oilseed protein meals and their derived products are deterrnined by the amino acid compositions, content of biologically active proteins, and various nonprotein constituents found in the defatted meals. Phytic acid (3), present as salts in all four meals, is beheved to interfere with dietary absorption of minerals such as 2inc, calcium, and iron (67) (see Food toxicants, naturally occurring Mineral nutrients). ... 

Bde salts, cholesterol, phosphoHpids, and other minor components are secreted by the Hver. Bile salts serve three significant physiological functions. The hydrophilic carboxylate group, which is attached via an alkyl chain to the hydrophobic steroid skeleton, allows the bile salts to form water-soluble micelles with cholesterol and phosphoHpids in the bile. These micelles assist in the solvation of cholesterol. By solvating cholesterol, bile salts contribute to the homeostatic regulation of the amount of cholesterol in the whole body. Bile salts are also necessary for the intestinal absorption of dietary fats and fat-soluble vitamins (24—26). 

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. 

Smaller pool sizes with normal semm B 2 levels may be maintained with dietary intakes below 1 pg. However, more substantial pool sizes are considered advantageous as protection against the development of pernicious anemia, which may occur in advanced age achlorhydria becomes more common after age 60, resulting in compromised absorption of vitamin 2-... 

Various mechanisms have been proposed to explain the hypocholesterolemic effect of GA (Annison et al., 1995 Tiss et al., 2001). Some studies have suggested that the viscosity of fermentable dietary fiber contributes substantially to the reduction of lipids in animals and humans (Gallaher et al., 1993 Moundras et al., 1994). However, other studies suggested that this property is not related to plasma lipids (Evans et al., 1992). The mechanism involved is clearly linked to increased bile acid excretion and fecal neutral sterol or a modification of digestion and absorption of lipids (Moundras et al., 1994). 

Although iron deficiency is a common problem, about 10% of the population are genetically at risk of iron overload (hemochromatosis), and elemental iron can lead to nonen2ymic generation of free radicals. Absorption of iron is stricdy regulated. Inorganic iron is accumulated in intestinal mucosal cells bound to an intracellular protein, ferritin. Once the ferritin in the cell is saturated with iron, no more can enter. Iron can only leave the mucosal cell if there is transferrin in plasma to bind to. Once transferrin is saturated with iron, any that has accumulated in the mucosal cells will be lost when the cells are shed. As a result of this mucosal barrier, only about 10% of dietary iron is normally absorbed and only 1-5% from many plant foods. 

Vitamin D is not strictly a vitamin since it can be synthesized in the skin, and under most conditions that is its major source. Only when sunlight is inadequate is a dietary source required. The main function of vitamin D is in the regulation of calcium absorption and homeostasis most of its actions are mediated by way of nuclear receptors that regulate gene expression. Deficiency—leading to rickets in children and osteomalacia in adults—continues to be a problem in northern latitudes, where sunlight exposure is poor. 

Pernicious anemia arises when vitamin B,2 deficiency blocks the metabohsm of folic acid, leading to functional folate deficiency. This impairs erythropoiesis, causing immature precursors of erythrocytes to be released into the circulation (megaloblastic anemia). The commonest cause of pernicious anemia is failure of the absorption of vitamin B,2 rather than dietary deficiency. This can be due to failure of intrinsic factor secretion caused by autoimmune disease of parietal cells or to generation of anti-intrinsic factor antibodies. 

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