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

It is well established that Giardia infection causes malabsorption. However, the precise mechanism of such a malabsorption is not known. To investigate this, transport studies, using the tissue accumulation technique, were carried out in mice infected with G. lamblia obtained from human stools. There was a significant fall in the transport of D-glucose, L-alanine and glycine in the infected animals compared with the controls. Kinetics of the D-glucose and glycine transport system were examined by measuring the tissue uptake in the presence of different concentrations of the substrate. For glucose, the affinity constant (Km) for the transport site was the same (4 . 37mM) in normal and infected animals but the maximal transport rate (V max) was considerably reduced in infected animals (158 . 7 mu moles/hr/g tissue) compared with (357 . 1 microgram moles/hr/g tissue) in controls. Results with glycine were similar; the Km was similar in control and infected animals (5 . 7 mM) whereas the V max was reduced in infected animals (27 . 02 microgram moles/hr/g tissue) compared with controls (45 . 5 micrograms moles/hr/g tissue). Analysis of the intestinal enzymes showed a significant decrease in the levels of brush border sucrase, lactase and alkaline phosphatase in infected animals; the cellular enzymes, LDH, GOT and GPT remained unaffected. The observed aberrations in the transport functions and brush border enzymes suggest that G. lamblia causes malabsorption by damaging the epithelial membrane of the enterocyte.
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PMID:Transport studies and enzyme assays in mice infected with human Giardia lamblia. 717 14

Congeneeital glucose-galactose malabsorption is a rare clinical entity transmitted by autossomic recessive gen. The defect is in the small intestinal active transport system which is shared by glucose and galactose. Diarrhea and failure to thrive from the first week of life are the prominent symptoms. We report two sibs from consaguineous parents with diarrhea and failure to thrive since they were born. Both children had glucose and galactose malabsorption but tolerated well formula containing fructose as the only source of carbohydrate. They showed flat blood glucose curves when tested with glucose and galactose loads but normal increments of the sugar blood levels with fructose load. The small intestinal biopsy performed in both patients revealed normal villous pattern. When put under a diet containing fructose as the only source of carbohydrate, both patients had their symptoms subsided and reassumed the normal pattern of growth.
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PMID:[Congential malabsorption of glucose and galactose in 2 brothers]. 718 24

The in vitro and in vivo production of hydrogen gas (H2) from various carbohydrates or proteins has been examined in normal rats and in rats infected with the nematode Nippostrongylus brasiliensis. Normal rat fecal homogenates were capable of producing H2 in vitro from glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate. Direct injection of glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate into the cecum of normal rats resulted in approximately twice as much H2 production in vivo than when these same carbohydrates or proteins were administered to the normal rats by gavage. Partial small intestinal villous atrophy was produced by infecting rats with the nematode N. brasiliensis. Impaired small intestinal cell function and evidence of malabsorption in the nematode-infected rats included: (a) decreased activity of intestinal cell lactase (-43%), sucrase (-33%), and alkaline phosphatase (-46%); (b) decreased gut sac uptake of 3-O-(methyl-3H]-D-glucose (-21%) or 1-[carboxyl-14C]-aminocyclopentane-1-carboxylic acid (-28%); and (c) increased (+ 64%-561%) 14CO2 production after D-[U-14C]xylose administration. These rats produced approximately twice as much H2 after gavage administration of glucose, sucrose, xylose, bovine serum albumin, or casein hydrolysate compared with normal rats. The present study suggests that H2 analysis may be useful in the evaluation of small intestinal malabsorption states in rats.
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PMID:Use of hydrogen gas (H2) analysis to assess intestinal absorption. Studies in normal rats and in rats infected with the nematode, Nippostrongylus brasiliensis. 728 87

A simple test is described for the diagnosis of monosaccharide malabsorption in infancy caused by a congenital defect of glucose and galactose transport. Increased hydrogen (H2) excretion in expired air after ingestion of sugar was used to diagnose this condition in an infant with severe diarrhoea after breast feeding. Abnormal amounts of H2 were excreted after oral administration of glucose and galactose, but not after fructose. A carbohydrate free diet supplemented with fructose resulted in rapid weight gain and disappearance of diarrhoea. The diagnosis of glucose-galactose malabsorption was confirmed by 14C-glucose transport studies on a jejunal mucosal biopsy specimen. These findings indicate that interval breath H2 estimation in mixed expired air is a non-invasive, reliable procedure for detection of monosaccharide malabsorption in infancy.
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PMID:Interval breath hydrogen test in glucose-galactose malabsorption. 731 38

Lactose malabsorption can be demonstrated by detecting hydrogen (H2) in the expired air after oral loading with lactose. A comparative study was carried out on 24 subjects. Following an oral loading dose of lactose, the H2 eliminated during expiration was assayed by gas chromatography, and blood galactose levels were measured. The results showed that the test was reliable, well tolerated and reproductible. However, the method does not measure the amounts of lactase present in the intestinal mucosa. The lactose loading test seems to be valuable for studies on lactose and carbohydrate malabsorption.
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PMID:[Lactase deficiency in the intestinal mucosa. Demonstration by hydrogen detection in the expired air after lactose loading (author's transl)]. 744 88

The study consisted of 172 subjects belonging to ethnic groups from Sinai in the Eastern Desert and the New Valley in the Western Desert, with respective mean ages of 36.7 +/- 2.0 and 26.6 +/- 1.0 years. Lactose absorption was assessed by measurement of urinary galactose in pooled 2-hr urine samples following ingestion of an oral lactose dose of 40 g. Mean 2-hr excretion values after ingestion were 32.3 mg galactose in the Sinai and 7.7 mg in the New Valley. In the evaluation of lactose malabsorption, a diagnosis of lactose malabsorption is based upon a cutoff point of 0.075 mg/mg urinary galactose:creatinine ratio. The overall prevalence rate in those populations is 34.3%. The proportion of lactose malabsorbers was 11.1% in Sinai and 51.0% in the New Valley. Highly significant differences (chi 2 = 29.5, P < 0.0001) were found between the two ethnic groups with regard to the frequency distribution of lactose malabsorption. The existence of an east-west gradient of increasing frequencies of lactose malabsorption gene is suggested.
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PMID:The frequency distribution of lactose malabsorption among adult populations from the eastern and western Egyptian deserts. 770 47

The article briefly describes the various methods that are available for diagnosing hypolactasia. Special attention is drawn to the fact that different methods are useful at different levels of the health care organization. When the test result indicates lactose malabsorption, general malabsorption should be excluded by a glucose-galactose tolerance test, for example. If the glucose-galactose tolerance test produces a normal result, it can be assumed that the patient has primary adult-type selective lactose malabsorption. The possibility of secondary lactose malabsorption must be excluded according to the principles described by Villako & Maaroos (104).
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PMID:Diagnosis of hypolactasia and lactose malabsorption. 804 16

Intestinal uptake of dietary glucose and galactose is mediated by the SGLT1 Na+/glucose cotransporter of the brush border. An SGLT1 missense mutation underlies hereditary glucose/galactose malabsorption, characterized by potentially fatal diarrhea; conversely, oral rehydration therapy exploits normal transport to alleviate life-threatening diarrhea of infectious origin. We have mapped the entire human SGLT1 Na+/glucose cotransporter gene from cosmid and lambda phage clones representing a genomic region of 112 kilobases. Transcription initiation occurred from a site 27 base pairs 3' of a TATAA sequence. All exon-flanking regions were sequenced, and the entire 112-kilobase region mapped with four restriction enzymes. SGLT1 is comprised of 15 exons (spanning 72 kilobases); a possible evolutionary origin from a six-membrane-span ancestral precursor via a gene duplication event is suggested from comparison of exons against protein secondary structure and from sequence considerations. A new missense mutation in exon 1 causing glucose/galactose malabsorption is also described. This is the first Na(+)-dependent cotransporter gene structure reported. These data facilitate the search for new glucose/galactose malabsorption-related mutations in this important gene and provide a basis for future evolutionary comparisons with other Na(+)-dependent cotransporters.
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PMID:Structure of the human Na+/glucose cotransporter gene SGLT1. 819 56

The Na+/glucose cotransporter gene SGLT1 encodes the primary carrier protein responsible for the uptake of the dietary sugars glucose and galactose from the intestinal lumen. SGLT1 transport activity is currently exploited in oral rehydration therapy. The 75-kDa glycoprotein is localized in the brush border of the intestinal epithelium and is predicted to comprise 12 membrane spans. In two patients with the autosomal recessive disease glucose/galactose malabsorption, the underlying cause was found to be a missense mutation in SGLT1, and the Asp28-->Asn change was demonstrated in vitro to eliminate SGLT1 transport activity. The SGLT1 gene was previously shown to reside on the distal q arm of chromosome 22 (11.2-->qter). We have used a cosmid probe for fluorescence in situ hybridization, which refines the localization to 22q13.1, and provide an example of the utility of the SGLT1 probe as a diagnostic for genetic diseases associated with translocations of chromosome 22.
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PMID:Assignment of the human Na+/glucose cotransporter gene SGLT1 to chromosome 22q13.1. 824 93

Intestinal absorption of glucose plays a key role in water economy as attested by the congenital and selective glucose and galactose malabsorption which is expressed as severe watery diarrhea just after birth, leading to life-threatening dehydration. This syndrome, transmitted on an autosomal recessive mode, is the consequence of a functional defect of the glucose-sodium cotransporter at the luminal membrane of the enterocyte of the small intestine. In one family, this defect was associated with a misense mutation at position 92 of the SGLT1 gene coding for the cotransporter. The mutant RNA reproduced the transport defect after injection in xenopus oocytes. These results confirm the genetic origin of the congenital defect; in addition they indicate that the study of the relationship between phenotype and genotype of congenital defects of intestinal transport may help in the understanding of basic intestinal functions in relation with human nutrition.
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PMID:[30 years' work on congenital glucose and galactose malabsorption: from phenotype to genotype]. 825 May 22


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