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

Ligand binding activity of intrinsic factor-cobalamin receptor (IFCR) was determined in homogenates and isolated brush-border membranes (BBM) of ileum and kidney from dogs exhibiting simple autosomal recessive inheritance of selective cobalamin malabsorption (Fyfe, J. C., Giger, U., Hall, C. A., Jezyk, P. F., Klumpp, S. A., Levine, J. S., and Patterson, D. F. (1991) Pediatr. Res. 29, 24-31). IFCR activity of affected dog ileal homogenates was 3-4-fold higher than normal whereas IFCR activity in affected dog kidney homogenates was one-tenth of normal. The recovery of IFCR activity in the BBM of ileum and renal cortex of affected dogs was 30- and 20-fold less than normal, respectively. The dissociation constant (Kd) for intrinsic factor-cobalamin was similar in BBM of both tissues and was the same in affected and normal dogs. In the affected dog ileal BBM, activities of alkaline phosphatase and sucrase-isomaltase and vesicular transport of glucose and Na(+)-taurocholate were normal. Immunoblots showed no IFCR cross-reactive material in the ileal or renal BBM of affected dogs. IFCR purified by affinity chromatography from kidney of both normal and affected dogs had an Mr = 230,000. However, amino acid analysis revealed that the affected dog IFCR had more lysine than the normal, and protease cleavage of the purified IFCRs revealed different peptide maps. Asparagine-linked oligosaccharides of both proteins were sensitive to peptide N-glycosidase F cleavage, but only the affected dog IFCR was endoglycosidase H sensitive. These results suggest that cobalamin malabsorption in this canine family is caused by inefficient BBM expression of IFCR due to a mutation of IFCR and its retention in an early biosynthetic compartment.
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PMID:Defective brush-border expression of intrinsic factor-cobalamin receptor in canine inherited intestinal cobalamin malabsorption. 199 30

Glucose/galactose malabsorption (GGM) is an autosomal recessive disease manifesting within the first weeks of life and characterized by a selective failure to absorb dietary glucose and galactose from the intestine. The consequent severe diarrhoea and dehydration are usually fatal unless these sugars are eliminated from the diet. Intestinal biopsies of GGM patients have revealed a specific defect in Na(+)-dependent absorption of glucose in the brush border. Normal glucose absorption is mediated by the Na+/glucose cotransporter in the brush border membrane of the intestinal epithelium. Cellular influx is driven by the transmembrane Na+ electrochemical potential gradient; thereafter the sugar moves to the blood across the basolateral membrane via the facilitated glucose carrier. We have previously cloned and sequenced a Na+/glucose cotransporter from normal human ileum and shown that this gene, SGLT1, resides on the distal q arm of chromosome 22. We have now amplified SGLT1 complementary DNA and genomic DNA from members of a family affected with GGM by the polymerase chain reaction. Sequence analysis of the amplified products has revealed a single missense mutation in SGLT1 which cosegregates with the GGM phenotype and results in a complete loss of Na(+)-dependent glucose transport in Xenopus oocytes injected with this complementary RNA.
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PMID:Glucose/galactose malabsorption caused by a defect in the Na+/glucose cotransporter. 200 13

The objective of this study was to investigate the mechanisms involved in intestinal absorption of fructose. The results indicate that adult rats readily absorbed 0.4 g of fructose, an amount equivalent to 1.4-1.6 g fructose/kg body wt. Acute malabsorption of fructose occurred with doses greater than 0.6 g (2.1-2.4 g/kg body wt). Continued exposure to dietary fructose resulted in a decrease in the evidence of colonic fermentation. Glucose or galactose administered with fructose enhanced the absorption of fructose. The greatest absorption was observed when equal amounts of fructose and glucose were given simultaneously. If glucose was ingested as a polymer (starch or dextrin), the stimulatory effect was dependent on the digestibility of the polymer. Sucrose given with the fructose and glucose diminished the absorption of fructose. Acarbazone, a specific inhibitor of alpha-glucosidases, including sucrase, also inhibited the facilitating effect of glucose and galactose in absorption of fructose. These results give evidence for joint absorption of the two monosaccharides, fructose and glucose.
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PMID:Intestinal absorption of fructose in the rat. 206 11

Oxidation of orally administered [13C]glucose and [13C]lactose and fecal recovery of malabsorbed substrates were determined in two groups of premature infants. Eighteen studies were performed with six infants at Johns Hopkins Hospital (JHH); 24 studies were performed with nine infants at Columbus Children's Hospital (CCH). The two groups differed in that JHH infants had shorter gestations but were older when studied. Fecal 13C loss after [13C]glucose administration did not differ between the two groups. Compared with glucose, the metabolism of lactose appeared to involve more malabsorption and colonic fermentation in JHH infants than in CCH infants and resulted in higher fecal losses of substrate carbon. Maturation appeared to involve increased proximal intestinal absorption and greater retention of absorbed carbohydrate. Simultaneous absorption of substrate from the small and large intestine may limit the usefulness of breath tests for 13C in the premature infant.
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PMID:Comparative absorption of [13C]glucose and [13C]lactose by premature infants. 210 54

Cases of malnutrition-related diabetes mellitus conforming to the description of the protein deficient pancreatic diabetes type in Ethiopian patients were compared with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic. Fourteen of 39 malnutrition-related diabetes mellitus patients had fat malabsorption compared with only two of ten Type 1 diabetic patients and one of nine control subjects. Xylose absorption was normal favouring a pancreatic cause for the malabsorption. Plasma C-peptide during oral glucose tolerance test was significantly lower than that in Type 2 diabetic patients and normal control subjects (p less than 0.01 to 0.001) and was also consistently but not significantly higher than in Type 1 diabetic patients. Glucagon secretion patterns were similar in malnutrition-related and Type 1 diabetic patients. Of 23 new malnutrition-related diabetic patients treated with glibenclamide after nutritional rehabilitation and insulin treatment, only three responded, 14 were unresponsive but remained ketosis free for over eight days while another six developed ketoacidosis or significant ketonuria within two to six days during the trial. Sixteen unselected Type 1 diabetic patients who discontinued their insulin therapy all developed frank ketoacidosis after a mean of 5.5 days. The similarity of the malnutrition-related and Type 1 diabetes mellitus in age of onset, insulin requirement for diabetic control and appearance of ketosis-proneness in some cases, together with the similarity of C-peptide and glucagon secretion patterns suggest that the protein deficient pancreatic diabetes variant of malnutrition-related diabetes mellitus may be Type 1 diabetes mellitus modified by the background of malnutrition rather than an aetiologically separate entity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical and hormonal (C-peptide and glucagon) profile and liability to ketoacidosis during nutritional rehabilitation in Ethiopian patients with malnutrition-related diabetes mellitus. 211

Cirrhotic patients often present muscle and adipose tissue depletion as well as reduced visceral protein concentration. Impaired absorption of nutrients may contribute to this altered nutritional status. To verify this hypothesis fecal fat excretion, intestinal mucosal function evaluated by means of the combined sugar oral load test, and intestinal clearance of alpha-1-Antirypsin were studied in 25 cirrhotic patients with clinical and biochemical signs of liver insufficiency and with portal hypertension. About 50% of the patients showed clinical evidence of malnutrition. Three of the 12 well-nourished, and 8 of the 13 malnourished patients presented significant steatorrhoea. Cirrhotics showed no impairment in mediated malabsorption and in passive permeability, as plasma D-xylose/3-O-methyl-glucose concentration and urinary lactulose/L-rhamnose excretion ratios were within the normal range. An increased value of alpha-1-Antitrypsin clearance was found only in two patients. These findings indicate that fat malabsorption is frequent in cirrhotic patients, particularly when malnourished, and does not depend on the presence of mucosal intestinal damage.
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PMID:Malabsorption and nutritional abnormalities in patients with liver cirrhosis. 213 41

The extent of carbohydrate digestion and absorption from two diets including either instant bean flakes (174 g/d) or potato flakes (102 g/d) was measured in seven ileostomy subjects during a 2-day period. Test foods contributed 40 per cent of the total dietary starch intake (160 g/d), the remainder coming from rice and white bread. Overall, 4 per cent and 0.7 per cent of the dietary starch consumed remained unabsorbed during the bean and potato periods, respectively. Between 9.0 and 10.9 per cent of dietary bean starch and less than 1.7 per cent of potato starch were not absorbed. Dietary fibre and resistant starch were completely recovered in ileostomy effluents. In separate meal tests with 40 g starch, beans gave lower blood glucose (P less than 0.05) and serum insulin (P less than 0.01) responses than potatoes. Dietary starch malabsorption from leguminous foods is less than previously estimated and does not explain the attenuated glycaemic and insulinaemic responses.
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PMID:Nutrients excreted in ileostomy effluents after consumption of mixed diets with beans or potatoes. II. Starch, dietary fibre and sugars. 217 Jan 4

The influence of pasta cooking time on starch digestion and plasma glucose and insulin responses was studied in 12 healthy subjects. During 3 consecutive days, one of three pasta test meals (50 g starch) cooked for 11, 16.5, and 22 min was served to each volunteer in a random order. Hydrogen and methane breath excretion was measured after pasta ingestion; plasma responses were compared with those of an equivalent oral glucose-tolerance test. No significant differences were found between cooking times and plasma indices, orocecal transit time, or incremental hydrogen excretion (delta peak hydrogen). With one exception, pasta meals that were completely absorbed were ingested by methane producers. Postprandial delta peak hydrogen was significantly lower in methane than in nonmethane producers (p less than 0.02). These results point to a lack of influence of cooking time on nutritional characteristics of pasta and suggest that starch malabsorption determined by breath-hydrogen-test criteria may be underestimated in methane producers.
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PMID:Pasta cooking time: influence on starch digestion and plasma glucose and insulin responses in healthy subjects. 217 90

Sibling cases of familial vitamin E deficiency accompanied by ataxia, polyneuropathy and mental retardation were reported. Case 1 was a 37-year-old male who developed progressive gait disturbance, deformity of the feet and head tremor from childhood, after normal delivery and development of early childhood. On physical examination, he had cataract, high arched palate and pes cavus. Neurological examination revealed mental retardation (WAIS 68), scanning speech, muscular atrophy of the face and extremities with predominance in the lower limbs, absent Achilles tendon reflex, disturbance of superficial and deep sensation predominant in distal limbs, and marked gait ataxia. Ataxia was both cerebellar and sensory in nature. Laboratory data of the blood showed no significant abnormalities including blood glucose and vitamin B12 except a markedly low level of serum vitamin E. The brain CT scan revealed severe cerebellar atrophy and marked dilatation of the cisterna magna and the subarachnoid space around the cerebellum. Motor nerve conduction velocity in the leg was decreased. Biopsy specimen from the quadriceps muscle showed neurogenic atrophy. Sural nerve biopsy revealed decrease in large myelinated fibers with axonal degeneration and regeneration. Oral administration of alpha-tocopherol acetate, 600 mg per day, diminished ataxia significantly. Based on lysosomal enzyme activity in leukocytes, clinical and laboratory examination, lipidosis or spinocerebellar degeneration was excluded. Chronic lipid malabsorption or beta lipoprotein deficiency which can cause decrease in vitamin E absorption, was not recognized. On oral loading with 2 g of alpha-tocopherol acetate, the decrease rate of serum vitamin E was normal. Consequently the low vitamin E was considered to have resulted from selective impairment of vitamin E absorption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial idiopathic vitamin E deficiency associated with cerebellar atrophy]. 226 7

Intestinal malabsorption of nutrients may be a critical factor in aging. For this reason, we investigated the nutrient absorption in mice of different ages of the life span, representing growth (3 mo), young adult (12 mo), mature (24 mo), old (30 mo), and very old (33-36 mo) periods. The everted sac technique was used to study the transepithelial transport of D-glucose, 3-O-methyl-D-glucose (3MG), and L-tyrosine. There was a 32% increase in the rate of D-glucose transepithelial transport during growth followed by a 55% decrease in the old mouse, and the same pattern occurred with 3MG, a nonmetabolized glucose derivative. However, L-tyrosine transepithelial transport was not impaired until the mouse reached the very old, 33-36 mo period. Also, the rate of D-glucose metabolism measured by lactate production in the very old mouse was only 45% of the mature mouse value. In addition, these transepithelial transport changes were accompanied by decreases in the number and the height of villi. The results indicate that intestinal transepithelial transport and the surface area for absorption decrease in aging.
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PMID:Intestinal transport during the life span of the mouse. 236 62


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