Vitamin protein intolerance

Propionyl CoA inhibits A(-acetylglutamate synthetase competitively with respect to acetyl CoA, forming A(-propionylglutamate and reducing the synthesis of A(-acetylglutamate. This is an obligatory activator of carbamyl phosphate synthetase, the first enzyme of urea synthesis. Vitamin B12 deficiency may result in some degree of protein intolerance and hyperammonemia. 

Normally there is very little fat in the feces. However, fat content in stools may increase because of various fat malabsorption syndromes. Such increased fat excretion is steatorrhea. Decreased fat absorption may be the result of failure to emulsify food contents because of a deficiency in bile salts, as in liver disease or bile duct obstruction (stone or tumor). Pancreatic insufficiency may result in an inadequate pancreatic lipase supply. Finally, absorption itself may be faulty because of damage to intestinal mucosal cells through allergy or infection. An example of allergy-based malabsorption is celiac disease, which is usually associated with gluten intolerance. Gluten is a wheat protein. An example of intestinal infection is tropical sprue, which is often curable with tetracycline. Various vitamin deficiencies may accompany fat malabsorption syndromes. 

The fourth section deals with various aspects Digestion, Absorption, and Nutritional Biochemistry. The chapter Obesity considers current problems with respect to the ever-increasing incidence of imbalance between energy intake and utilization. Key problems of undemutrition are discussed in the chapters Protein-Energy Malnutrition and Vitamin A Deficiency in Children. The chapters Lactose Intolerance, Pancreatic Insufficiency, and Abetalipoproteinemia focus on the biochemical processes underlying food digestion and absorption. Calcium Deficiency Rickets, Vitamin B12 Deficiency, and Hemochromatosis provide discussions of absorption and utilization of vitamin D, vitamin B12, and iron, respectively. 

Soy-based formulas were developed for infants perceived to be intolerant of cow-milk protein. The first soy formulas were commercially available in 1929 (Abt, 1965). These formulas were made with soy flour and were not well accepted by parents, who complained of loose, malodorous stools, diaper rash, and stained clothing. In the mid-1960s isolated soy protein was introduced into formulas. These formulas were much more like milk-based formulas in appearance and acceptance. However the preparation of isolated soy protein resulted in the elimination of most of the vitamin K in the soy, and a few cases of vitamin K deficiency were reported. The occurrence of nutrient deficiencies in infants fed milk-free formulas contributed to the development of federal regulations concerning the nutrient content of formulas (Fomon, 1993). Soy formulas now account for about 40 percent of formula sales in the United States. Some parents want to avoid cow-milk protein in the diet and thus wean directly to soy without any reported intolerance to cow-milk formulas. While formulas containing extensively hydrolyzed protein have long been available for infants with allergy to intact cow-milk protein, formulas with protein that is not as completely hydrolyzed have recently been introduced for normal-term infants. 

Nutrition is utilized to provide general support for the debilitated patient with a chronic illness. Often, patients are deficient in protein, calories, potassium, vitamins, etc. The healing process is impaired by poor nutrition and is enhanced by proper nutrition. In some cases enteral nutrition is not practical or is impossible. With the techniques of total parenteral nutrition, it is now possible to provide nutritional support for almost all types of patients. Specific nutritional therapy is necessary in certain types of metabolic and related diseases. Nutritional therapy is essential in conditions where specific food intolerances are the basis for a disease. 

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