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Query: UMLS:C0024523 (
malabsorption
)
7,319
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID:[30 years' work on congenital glucose and galactose malabsorption: from phenotype to genotype]. 825 May 22
1. A vicious cycle of
malabsorption
and malnutrition has been implicated in the pathogenesis of protracted diarrhoeal disease in infancy. Vitamin E deficiency is common in malnourished infants with protracted diarrhoea. We have studied the effects of chronic vitamin E deficiency on small-intestinal secretion and absorption in the rat. 2. Weanling rats were fed vitamin E-sufficient or -deficient diets for 21 weeks. Jejunal function was studied in vitro in an Ussing chamber after this period. 3. Steady-state isotopic flux experiments in unstimulated tissues demonstrated net
Na+
and Cl- secretion in vitamin E-deficient jejuna but net
Na+
and Cl- absorption in vitamin E-sufficient jejuna. 4. Basal intestinal short-circuit current was the same in both groups. 5. Cyclic nucleotide and maximal non-neuronal acetylcholine-mediated electrogenic secretion were increased in vitamin E-deficient jejuna. 6. Exogenous 5-hydroxytryptamine (serotonin) induced a smaller increment in electrogenic secretion in vitamin E-deficient jejuna. 7. Vitamin E-deficient jejuna were less responsive to exogenous noradrenaline, resulting in a smaller alpha 2-adrenergic-mediated decrease in intestinal short-circuit current. 8. Fasting for 72h produced a greater increment in intestinal short-circuit current in vitamin E-deficient jejuna. 9. Chronic vitamin E deficiency is prosecretory in the small intestine and may predispose to the perpetuation of protracted diarrhoeal diseases.
...
PMID:Modulation of small-intestinal secretion and absorption in chronic vitamin E deficiency: studies in rat jejunum in vitro. 828 52
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 missense 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.
...
PMID:[Thirty years of research on congenital glucose and galactose malabsorption: from phenotype to genotype]. 831 9
Cotransporters harness ion gradients to drive 'active' transport of substrates into cells, for example, the Na+/glucose cotransporter (SGLT1) couples sugar transport to
Na+
gradients across the intestinal brush border. Glucose-Galactose
Malabsorption
(GGM) is caused by a defect in SGLT1. The phenotype is neonatal onset of diarrhea that results in death unless these sugars are removed from the diet. Previously we showed that two sisters with GGM had a missense mutation in the SGLT1 gene. The gene has now been screened in 30 new patients, and a heterologous expression system has been used to link the mutations to the phenotype.
...
PMID:Defects in Na+/glucose cotransporter (SGLT1) trafficking and function cause glucose-galactose malabsorption. 856 65
Short-bowel syndrome is a state of severe
malabsorption
secondary to extensive bowel resection. The most common reasons for extensive bowel resection are Crohn's disease and mesenteric infarction. The pathophysiological consequences depend on extent and site of resection, integrity and adaptation of the remaining bowel, and secondary effects on other organs. Most extensively bowel resected patients can be adequately nourished by mouth, especially since they develop compensatory hyperphagia. For patients with colon in function a high-carbohydrate low-fat diet is beneficial compared to a diet with a normal fat content, because it results in decreased diarrhoea, decreased faecal mineral losses, and increased energy assimilation. The relative amount of dietary fat does not influence stool mass or energy assimilation in jejunostomy patients. Patients with jejunostomy have a high faecal output of water,
sodium
, and divalent cations, and they often need permanent parenteral supply of saline as well as calcium and magnesium if their small intestinal remnant is < 200 cm and parenteral nutritional support if they retain < 100 cm small bowel. In contrast, 50 cm of the jejunum often suffices for adequate oral nutrition if most of the colon is preserved. The majority of patients needing long-term intravenous supply are trained to administer parenteral nutrition at home (HPN). Most patients on HPN obtain a good or fair quality of life with hospital readmissions corresponding to an average of 10% of the HPN duration and an overall HPN related mortality of about 4%.
...
PMID:Nutrition in short-bowel syndrome. 872 85
Fermentation, the process whereby anaerobic bacteria break down carbohydrates to short-chain (C2-C6) fatty acids (SCFAs), is an important function of the large bowel. SCFAs constitute approximately two-thirds of the colonic anion concentration (70-130 mmol/l), mainly as acetate, propionate, and butyrate. Gastroenterologists have, in spite of these facts, addressed this scientific field surprisingly late, in contrast to veterinarians, for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades. Interest in the effects of SCFA production on the human organism has been growing rapidly in the last 10 years, because gastrointestinal functions and beneficial effects are associated with these acids. SCFAs are of major importance in the understanding of the physiological function of dietary fibre and their possible role for colonic neoplasia. SCFA production and absorption are closely related to the nourishment of the colonic mucosa and
sodium
and water absorption, and mechanisms of diarrhoea. Patients with severe
malabsorption
compensate by the fermentation of otherwise osmotic active saccharides to SCFAs, which are readily absorbed and used as energy fuels in the organism. SCFA production from dietary carbohydrates is a mechanism whereby considerable amounts of calories can be salvaged in short-bowel patients with remaining colonic function if dietary treatment is adjusted. SCFA enemas are a new and promising treatment modality for patients with ulcerative colitis. The effect has been attributed to the oxidation of SCFAs in the colonocytes. An impressive number of papers have described the effects of butyrate on various cell functions, the significance of which is still unknown. Up until now, attention has been related especially to cancer prophylaxis and treatment. Diminished production of SCFAs appears to be involved in antibiotic-associated diarrhoea, diversion colitis, and possibly in pouchitis. The interaction between bacterial fermentation, ammonia metabolism, and bacterial growth and protein synthesis appears to be the main mechanism of action of lactulose treatment in hepatic coma. Pathological and extremely high rates of saccharide fermentation explain the severe deterioration in patients with D-lactate acidosis. Hence, this scientific field has come late to clinical working gastroenterologists, but as work is progressing the production of SCFAs in the large bowel becomes involved in several well-known intestinal disorders.
...
PMID:Short-chain fatty acids in the human colon: relation to gastrointestinal health and disease. 872 86
1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental
sodium
and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need
sodium
restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for
malabsorption
and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term
sodium
restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
...
PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44
In the newborn, sugars present in human milk and formulas are assimilated by both small intestinal digestion and, especially in the case of lactose, colonic bacterial fermentation. Colonic fermentation of carbohydrate serves three major functions: (1) conservation of a fraction of the metabolizable energy of dietary carbohydrate that is not absorbed in the small intestine; (2) prevention of osmotic diarrhea; and (3) production of short-chain fatty acids that stimulate
sodium
and water absorption, serve as fuel for colonocytes, and stimulate cell replication in colon and small intestine. Diarrhea produced in association with small bowel
malabsorption
of sugar may be caused by three, potentially overlapping mechanisms: (1) osmotic effects of unfermented sugar, which may cause secondary disruption of fermentation by purging the bacteria or diluting the bacteria mass; (2) damage to the colon mucosa from excessive fermentation leading to SCFA
malabsorption
and osmotic diarrhea on this basis; and (3) excessive fermentation leading to lowering of luminal pH and inhibition of bacterial enzymes. Therapy aimed at reducing diarrhea associated with sugar
malabsorption
might involve either slowing of motility to facilitate fermentation or stimulation of fermentative activity, but such interventions would depend on greater understanding of the mechanisms for colonic dysfunction in this condition.
...
PMID:Digestion, absorption, and fermentation of carbohydrates in the newborn. 878 Sep 2
Because selenium is seldom added to formulations for enteral nutrition (EN), postoperative patients who are supported with EN are at risk for selenium deficiency. This report describes four cases of suspected selenium deficiency in long-term EN. Two patients underwent pancreaticoduodenectomy, one underwent total gastro-pancreatectomy, and one underwent esophageal resection and reconstruction with jejunal autotransplantation. They all developed
malabsorption syndrome
within 2 yr after operation. Enteral nutritional support with an elemental diet was provided continuously for 7-11 yr. Over the past 1-2 yr they experienced increasing bilateral muscular pain and weakness in the legs, gait disturbance, palpitation, and shortness of breath. Investigation for possible trace element deficiency revealed very low levels of selenium in the blood. After 10-20 d of supplementation with daily intravenous administration of selenious acid 0.16 mg/d (100 micrograms/d of selenium), their blood levels of selenium rose and their symptoms resolved. They were then continued on a maintenance regimen of oral
sodium
selenite 0.13 mg/d (60 micrograms/d of selenium).
...
PMID:Four cases of selenium deficiency in postoperative long-term enteral nutrition. 883 35
At the Diarrhoeal Disease Research and Rehydration Centre of Bab El-Sha'reya Hospital in Cairo, Egypt, clinical researchers randomly assigned 90 fully weaned boys aged 3-24 months with non-cholera diarrhea and signs of moderate dehydration to either the treatment group receiving the standard glucose-based oral rehydration solution (ORS) or the group receiving a reduced-osmolarity ORS with minimally hydrolyzed maltodextrins (MD) (50 g/l) in place of glucose (20 g/l). They wanted to determine whether the reduced-osmolarity, MD-based ORS yielded similar benefits as the glucose-based ORS and to examine the effect of sugar
malabsorption
on the efficacy of both solutions. The osmolarity of the MD-based ORS was 227 mmol/l compared to 311 mmol/l for the standard ORS. There were no significant differences in the clinical outcomes (duration of diarrhea, stool output, ORS intake, serum
sodium
level, and weight gain at discharge) for each treatment group. High stool output had a significant positive association with longer duration of diarrhea (33 vs. 15 hours for low stool output; p 0.01), a persistently elevated serum
sodium
concentration (149 vs. 144 mmol/l for low stool output; p 0.02), the need for intravenous infusion (11/41 vs. 0/48 for low stool output; p 0.002), and an increase in substances that reduce feces (10.8 vs. 3.4 g/l for low stool output; p 0.001). Based on these findings, the researchers hypothesized that, like the standard ORS, the reduced osmolarity ORS, in which glucose is replaced with MD, also caused sugar
malabsorption
. The sugar
malabsorption
, in turn, increased the effective intraluminal osmolarity to equal or exceed that of the standard ORS. Both sugar
malabsorption
and intraluminal hypertonicity were responsible for a net flow of water from extracellular fluid into the gut, an increased serum
sodium
concentration, increased thirst leading to greater intake of ORS, ORS treatment failure, an increase in stool output, and an increase in duration of diarrhea. In conclusion, reduced-osmolarity, glucose-based ORS is superior to the standard glucose-based ORS and reduced-osmolarity, MD-based ORS.
...
PMID:Efficacy of standard glucose-based and reduced-osmolarity maltodextrin-based oral rehydration solutions: effect of sugar malabsorption. 900 27
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