Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary carbohydrates, which constitute a most important source of equine nutrition, are digested and absorbed by a series of complex processes principally in the small intestine, beginning with intraluminal starch hydrolysis by the action of pancreatic amylase. The continuous secretion of a copious volume of pancreatic juice, low in enzyme activity, presumably releases sufficient oligosaccharides for further hydrolysis at the intestinal cell surface by brush border enzymes. Active carrier mediated mechanisms then transport the final hexose products across the intestinal cell for uptake in the hepatic portal system. Brush border disaccharidase activities in the equine small intestine are of the same order of magnitude, and have a similar distribution pattern, to those reported in omnivorous and carnivorous species. The disaccharidase development patterns are characteristic and reflect the ability of the horse to digest the major nutrient sources adequately at various stages of life. The efficiency of the mucosal disaccharidases and the monosaccharide transport systems in the equine small intestine have been established by a series of oral disaccharide and monosaccharide tolerance tests. Horses older than three years of age are unable to hydrolyse lactose, but young and adult horses are fully capable of rapidly hydrolysing sucrose and maltose loads. Several tests have clinical application for assessing small intestinal dysfunction in the investigation of diarrhoea and malabsorption. The deficient digestion or absorption of carbohydrate, whether primary or secondary, can almost always be localized to a defect in the enzymic or transport capacity of the small intestinal surface cell. The continued ingestion of lactose could be detrimental in severely diarrhoeic foals.
 ...
PMID:Carbohydrate digestion and absorption in the equine small intestine. 110 Aug 25

Fructose, a naturally occurring monosaccharide, is increasingly used as an added sweetener in processed foods in the form of high fructose corn syrup. Increased fructose intake combined with the identification of children with clinical evidence of isolated fructose malabsorption (IFM) has stimulated interest in possible disorders of fructose absorption. The intestinal absorption of fructose is carried out by the facilitative hexose transporter, which has been designated as GLUT5. Functional properties and tissue distribution of GLUT5 suggest that IFM might be due to mutations in the GLUT5 gene. To test this hypothesis, we screened the GLUT5 gene for mutations in a group of eight patients with IFM and in one subject with global malabsorption, as compared with 15 healthy parents of subjects and up to 6 unrelated controls. No mutations were found in the protein coding region of this gene in any of the subjects. A single G to A substitution in the 5' untranslated region of exon 1 was identified in the subject with global malabsorption. This subject and her healthy mother were heterozygous for the variant sequence, suggesting that it was unlikely to be clinically significant. In addition, sequence analysis of each of the 12 GLUT5 exons was performed in the index case and confirmed the negative single-strand conformation polymorphism findings. These studies demonstrate that IFM does not result from the expression of mutant GLUT5 protein.
 ...
PMID:Molecular analysis of the fructose transporter gene (GLUT5) in isolated fructose malabsorption. 894 59

Carcinogenic and other toxic manifestations of areca/betel nut extracts on the buccal cavity and upper digestive tract are well documented. The present study deals with in vivo and in situ effects of aqueous and alcoholic extracts of areca nut on rat intestinal epithelial cell membrane. In vivo daily oral administration by gastric intubation for 1p w produced significant declines in brush border membrane alkaline phosphatase, Ca2+-Mg2+-ATPase, and the digestive enzyme sucrase. The decline in activities were more prominent after 4-w exposures. Instant short term in situ exposure to aqueous extract produced higher enzyme activities, indicating the initial activation of active sites by areca nut extract constituent(s). Significant declines in brush border membrane constituents (total hexose, sialic acid and cholesterol) were also evident following continuous exposures to areca nut extracts. These findings suggest that prolonged chewing of areca nut causes significant alterations in intestinal epithelial cell lining functions and could lead to malabsorption of nutrients.
 ...
PMID:Effect of betel/areca nut (Areca catechu) extracts on intestinal epithelial cell lining. 1100 13

Fructose is found widely in the diet as a free hexose, as the disaccharide, sucrose and in a polymerized form (fructans). Free fructose has limited absorption in the small intestine, with up to one half of the population unable to completely absorb a load of 25 g. Average daily intake of fructose varies from 11 to 54 g around the world. Fructans are not hydrolysed or absorbed in the small intestine. The physiological consequences of their malabsorption include increasing osmotic load, providing substrate for rapid bacterial fermentation, changing gastrointestinal motility, promoting mucosal biofilm and altering the profile of bacteria. These effects are additive with other short-chain poorly absorbed carbohydrates such as sorbitol. The clinical significance of these events depends upon the response of the bowel to such changes; they have a higher chance of inducing symptoms in patients with functional gut disorders than asymptomatic subjects. Restricting dietary intake of free fructose and/or fructans may have durable symptomatic benefits in a high proportion of patients with functional gut disorders, but high quality evidence is lacking. It is proposed that confusion over the clinical relevance of fructose malabsorption may be reduced by regarding it not as an abnormality but as a physiological process offering an opportunity to improve functional gastrointestinal symptoms by dietary change.
 ...
PMID:Review article: fructose malabsorption and the bigger picture. 1721 53

Fructose is a hexose sugar that is being increasingly consumed in its monosaccharide form. Patients who exhibit fructose malabsorption can present with gastrointestinal symptoms that include chronic diarrhea and abdominal pain. However, with no clearly established gastrointestinal mechanism for fructose malabsorption, patient analysis by the proxy of a breath hydrogen test (BHT) is controversial. The major transporter for fructose in intestinal epithelial cells is thought to be the facilitative transporter GLUT5. Consistent with a facilitative transport system, we show here by analysis of past studies on healthy adults that there is a significant relationship between fructose malabsorption and fructose dose (r = 0.86, P < 0.001). Thus there is a dose-dependent and limited absorption capacity even in healthy individuals. Changes in fructose malabsorption with age have been observed in human infants, and this may parallel the developmental regulation of GLUT5 expression. Moreover, a GLUT5 knockout mouse has displayed the hallmarks associated with profound fructose malabsorption. Fructose malabsorption appears to be partially modulated by the amount of glucose ingested. Although solvent drag and passive diffusion have been proposed to explain the effect of glucose on fructose malabsorption, this could possibly be a result of the facilitative transporter GLUT2. GLUT5 and GLUT2 mRNA have been shown to be rapidly upregulated by the presence of fructose and GLUT2 mRNA is also upregulated by glucose, but in humans the distribution and role of GLUT2 in the brush border membrane are yet to be definitively decided. Understanding the relative roles of these transporters in humans will be crucial for establishing a mechanistic basis for fructose malabsorption in gastrointestinal patients.
 ...
PMID:Intestinal fructose transport and malabsorption in humans. 2114 1