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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose Galactose Malabsorption is a genetic disorder caused by a defect in glucose and galactose transport across the intestinal brush border. Normally, lactose in milk is broken down into glucose and galactose by lactase, an ectoenzyme on the brush border, and the hexoses are transported into the cell by the Na+-glucose cotransporter SGLT1. The mutations causing the defect in sugar transport have been identified in patients from 33 kindreds, and functional studies have established how these mutations cause the disease.
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PMID:I. Glucose galactose malabsorption. 981 14

Bioavailability of diltiazem was investigated in rats with the neomycin induced malabsorption syndrome in presence of surfactants. Tween 80, sodium lauroyl sulphate and lecithin were added under their critical miscellar concentration levels. Increases of diltiazem bioavailability (in the range of 5-29%) promoted by additions of the surfactants were observed.
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PMID:Enhancement of diltiazem bioavailability by traces of surfactants in rats after neomycin-induced malabsorption syndrome. 983 46

Whether carbohydrate malabsorption causes diarrhea probably depends on the balance between the osmotic force of the carbohydrate and the compensatory capacity of the colon to dispose of the carbohydrate by bacterial fermentation. The present study evaluated the specific role of the osmolarity by comparing the severity of diarrhea after ingestion of two nonabsorbable carbohydrates, the fructooligosaccharide Idolax and the disaccharide lactulose. Both carbohydrates are readily fermented by the colonic flora but differ in osmolarity, the osmotic force being twice as high for lactulose as for Idolax. Twelve subjects were given increasing doses (0, 20, 40, 80, 160 g/d) of Idolax and lactulose in a crossover design. Every dose level was administered for three days with intervals of one week. Stools were collected on the third day to determine 24-hr volume, concentrations of short-chain fatty acids, L- and D-lactate, residues of Idolax or lactulose, sodium, potassium, pH, osmolarity, and in vitro productions of organic acids. Measured by short-chain fatty acid and lactate formation in a fecal incubation system, the fermentation of Idolax and lactulose was identical and very rapid compared with a range of reference carbohydrates. A laxative effect of both Idolax and lactulose was demonstrated. The increment in fecal volume as a function of the dose administered was twice as high for lactulose (slope of the regression line = 7.3, r = 0.64, P< 10(-5)) as for Idolax (slope = 3.7, r = 0.51, P<10(-3)), i.e., isosmolar doses of lactulose and Idolax had the same effect on fecal volume. The variation in fecal volume was substantial (lactulose 80 g/day: 110-1360 g/day; Idolax 160 g/day: 130-1440 g/day). High responders had earlier and larger fecal excretions of the saccharide compared with low-responders. Fecal volume in carbohydrate-induced diarrhea is proportional to the osmotic force of the malabsorbed saccharide, even though all or the majority of the saccharide is degraded by colonic bacteria. The capacity to modify the diarrhea varies considerably from person to person and is associated with colonic saccharide disposal, whereas the variation in response to isosmolar amounts of different saccharides is small within the same individual.
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PMID:Comparison of diarrhea induced by ingestion of fructooligosaccharide Idolax and disaccharide lactulose: role of osmolarity versus fermentation of malabsorbed carbohydrate. 988 2

Loss of bone is an almost universal accompaniment of aging that proceeds at an average rate of 0.5-1% per annum from midlife onwards. There are at least four nutrients involved in this process: calcium, salt, protein, and vitamin D, at least in women. The pathogenesis of osteoporosis in men is more obscure. Calcium is a positive risk factor because calcium requirement rises at the menopause due to an increase in obligatory calcium loss and a small reduction in calcium absorption that persist to the end of life. A metaanalysis of 20 calcium trials shows that this process can generally be arrested by calcium supplementation, although there is some doubt about its effectiveness in the first few years after menopause. Salt is a negative risk factor because it increases obligatory calcium loss; every 100 mmol of sodium takes 1 mmol of calcium out of the body. Restricting salt intake lowers the rate of bone resorption in postmenopausal women. Protein is another negative risk factor; increasing animal protein intake from 40 to 80 g daily increases urine calcium by about 1 mmol/day. Low protein intakes in third world countries may partially protect against osteoporosis. Vitamin D (sometimes called a nutrient and sometimes a hormone) is important because age-related vitamin D deficiency leads to malabsorption of calcium, accelerated bone loss, and increased risk of hip fracture. Vitamin D supplementation has been shown to retard bone loss and reduce hip fracture incidence in elderly women.
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PMID:Nutrition, osteoporosis, and aging. 992 42

Effective clinical therapy to augment intestinal absorption of water and electrolytes does not exist; the gut hormone, peptide YY (PYY), is a potent proabsorptive agent in animal models. The purpose of our study was to evaluate the effects of two novel PYY analogs, BIM-43073D and BIM-43004C, on intestinal absorption. Dogs with ileal Thiry-Vella fistulae (TVF) were treated with either PYY, BIM-43073D, or BIM-43004C. Administration of BIM-43073D significantly increased water and sodium absorption over baseline and maintained this level of increased absorption for a longer duration than an equimolar dose of PYY. Administration of BIM-43004C significantly increased sodium and water absorption over baseline at a level equal to that of PYY. The novel PYY analogs, BIM-43073D and BIM-43004C, are effective proabsorptive agents with BIM-43073D producing more sustained effects than PYY. These compounds may be clinically useful in the treatment of gut malabsorption in conditions such as cholera, Crohn's disease, and the short-bowel syndrome.
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PMID:Characterization of two novel proabsorptive peptide YY analogs, BIM-43073D and BIM-43004C. 1008 Jan 63

Ileal Na+-dependent bile acid transporter (ISBT) constituting a gateway to enterohepatic circulation of bile acids occurs exclusively at the distal site of the small intestine. In the present study, we examined colonic tumorigenesis promoted by deoxycholic acid in relation to the expression of the ISBT. For this purpose, the small intestine of a Fischer-344 rat was resected a length of 20 cm above the ileo-cecal valve (ileal resection) or below the duodenum (jejunal resection). Then, rats were treated with an intraperitoneal injection of azoxymethane (15 mg/kg body wt.) once a week for 3 weeks and fed a 20% casein diet supplemented with 0.2% deoxycholate for 39 weeks. Northern blot analysis demonstrated that the ISBT mRNA was hardly detectable in ileum-resected rats. The excretion of fecal bile acids was 1.5-fold higher in the ileum-resected group than in the jejunum-resected group (P < 0.05). On the contrary, the serum bile acids concentration of ileal-resected rats was about one-half of that of jejunum-resected animals (P < 0.05). The tumor incidence and the total tumor number were significantly higher in the ileum-resected group than in the jejunum-resected one (P < 0.05). Interestingly, no tumor was found at the proximal colon in the jejunum-resected group while tumors developed frequently at the proximal site as well as mid and distal colon in the ileum-resected group. These observations demonstrate that malabsorption of bile acids owing to the lack of ISBT enhanced colon tumorigenesis.
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PMID:Elimination of Na+-dependent bile acid transporter from small intestine by ileum resection increases [correction of increase] colonic tumorigenesis in the rat fed deoxycholic acid. 1053 Jul 78

Tropical grain legumes represent potentially important feed for farm animals. However, diarrhoea and poor growth performance have been reported, due to the various anti-nutritional factors they contain. This study addressed in particular whether dietary cowpea impaired the growth of pigs, whether the small intestinal Na+/D-glucose coabsorptive transport capacity was decreased, whether the Cl- secretory capacity was increased, and, finally, whether these parameters were affected by heat treatment of cowpea. Pigs, 4 weeks old, were fed for 3 weeks with one of three diets: (i) standard soy, (ii) 75% of soy substituted with raw cowpea, or (iii) 75% of soy substituted with heat-treated cowpea. The absorptive and secretory capacities of the jejunum and ileum were measured with the Ussing chamber technique. Weight gain, feed intake, pancreatic protein and enzyme concentrations and levels of the blood hormones glucagon and cholecystokinin were also measured. The Na+ transport capacity was measured as the increase in short-circuit current (Isc) when D-glucose was added to the luminal side in the Ussing chambers. Isc was significantly higher in the jejunum from raw cowpea-fed pigs than in the jejunum from standard soy-fed pigs, with no difference between the two cowpea-fed groups. The phosphodiesterase inhibitor theophylline was subsequently added bilaterally, and the increase in Isc indicated the cAMP-depedent Cl- secretory capacity. In the jejunum this was significantly higher in raw and heat-treated cowpea-fed pigs than in standard soy-fed pigs. In contrast, there were no differences in the ileal transport capacities. There were no differences in the pancreatic protein and trypsin concentrations or the blood hormones, but the raw cowpea-fed pigs had significantly lower pancreatic amylase than standard soy-fed pigs. Weight gain and feed intake were lowest in the cowpea-fed groups, with no significant difference between the two groups. In conclusion, the hypothesis of impaired small intestinal absorption of D-glucose and Na+ as causing malabsorption, and therefore impaired growth, during cowpea substitution in the feed may be firmly rejected. The increased Cl- secretory capacity, although moderate, may contribute to the higher incidence of post-weaning diarrhoea in cowpea-fed pigs, as observed in other studies. Additionally, the decreased food intake, feed conversion and weight gain were unaffected by heat treatment, further suggesting involvement of heat-stable anti-nutritional factors.
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PMID:Effects of dietary substitution with raw and heat-treated cowpea (Vigna unguiculata) on intestinal transport and pancreatic enzymes in the pig. 1063 95

A 51-year-old woman who had been treated with levothyroxine sodium because of hypothyroidism after total thyroidectomy for thyroidal cancer was admitted to our hospital for persistent hypothyroidism despite large dose administration of levothyroxine (600 microg/day). The patient complained of severe general fatigue and body weight gain. Free thyroxine, free triiodothyronine and thyrotropin levels were 0.97 ng/dl, 1.55 pg/ml and 24.51 microU/ml, respectively, under oral administration of levothyroxine. Levothyroxine loading test performed by liquid form, pulverized tablets via nasogastric tube and intravenous administration revealed no evidence of malabsorption or metabolic disorder of levothyroxine, although oral intake of tablets was ineffective due to her factitiousness. We report here a possible case of "pseudomalabsorption of levothyroxine" to emphasize the clinical recognition of this disorder in patients with resistant hypothyroidism.
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PMID:Pseudomalabsorption of levothyroxine: a case report. 1081 Dec 92

There are two mechanisms for glucose transport across cell membranes. In the intestine and renal proximal tubule, glucose is transported against a concentration gradient by a secondary active transport mechanism in which glucose is cotransported with sodium ions. In all other cells, glucose transport is mediated by one or more of the members of the closely related GLUT family of glucose transporters. The pattern of expression of the GLUT transporters in different tissues is related to the different roles of glucose metabolism in different tissues. Primary defects in glucose transport all appear to be extremely rare and not all possible deficiencies have been identified. Deficiency of the secondary active sodium/glucose transporters result in glucose/galactose malabsorption or congenital renal glycosuria. GLUT1 deficiency produces a seizure disorder with low glucose concentration in cerebrospinal fluid and GLUT2 deficiency is the basis of the Fanconi-Bickel syndrome, which resembles type I glycogen storage disease.
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PMID:Glucose transporters: structure, function and consequences of deficiency. 1086 40

Two young females with severe morbid obesity presented with Wernicke's syndrome after Roux-en-Y gastro-jejunum bypass had been performed. The first patient had recurrent vomiting and dyplopia two months post-surgery. Physical examination indicated bilateral ophthalmoparesia with conserved convergence and ataxia. The second patient had frequent vomiting episodes over the previous three months together with lower limb hypotonia, myoclonia and generalised tonicoclonic seizures on two occasions within one year of surgery. In both cases routine blood test, ion levels (sodium, potassium, calcium, phosphates), electroencephalogram and CT scan were normal. Thiamine therapy was instigated on the basis of clinical intuition and the first patient achieved complete remission within 24 hours while the second improved gradually in that two years later only mild lower limb hypotonia and a slight cognitive deficit remains. Erythrocyte transketolase activity determinations were abnormal on two separate occasions for this second patient. Vitamin B1 determinations were not available for the first patient. In conclusion, the restriction in energy intake and the persistent vomiting together with malabsorption induced by the surgical intervention could explain the vitamin deficiency causing Wernicke's encephalopathy. This indicates a need for close monitoring and systematic vitamin supplementation in those patients who undergo bariatric surgery.
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PMID:Wernicke's syndrome after bariatric surgery. 1103 Oct 78


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