Disorders of intestinal amino - acid transport

There are obvious analogies between disorders of intestinal amino-acid absorption and the more familiar anomalies of carbohydrate absorption. Both monosaccharides and free amino acids are important water-soluble nutrients which must be transported across the lipid-containing intestinal cell membrane by specific active transport processes involving concentration of the compounds within the cell cytoplasm above that of the intestinal lumen or the portal capillary blood. Reduced efficiency of carbohydrate absorption may be due to four possible types of defect: (1) reduced intraluminal hydrolysis of polysaccharides, eg, in pancreatic insufficiency; (2) inefficiency of the active transport process from the lumen to the brush border of the mucosal cell, eg, in hereditary glucose-galactose malabsorption; (3) deficiency or absence of lactase or of sucrase at the brush border of the enterocyte, eg, acquired lactase deficiency; and (4) toxic factors reducing the efficiency of carbohydrate transport, eg, fructose intolerance. Corresponding factors account for diseases resulting in a reduced efficiency of absorption of the products of protein digestion. One obvious difference between the two types of disease, however, is the more severe diarrhoea produced by carbohydrate malabsorption. Unabsorbed sugars in the colon cause severe osmotic diarrhoea associated with frothy and highly acidic stools. The carbohydrates are partly converted to organic acids within the colonic lumen, and the stool pH may be lower than 4 0. By contrast, unabsorbed amino acids are almost always in too low concentration to produce osmotic diarrhoea, and their degradation products have not been proved to cause any toxic effects.