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Assignment of the locus for congenital lactase deficiency to 2q21, in the vicinity of but separate from the lactase-phlorizin hydrolase gene.

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Congenital lactase deficiency (CLD) is an autosomal recessive, gastrointestinal disorder characterized by watery diarrhea starting during the first 1-10 d of life, in infants fed lactose-containing milks. Since 1966, 42 patients have been diagnosed in Finland. CLD is the most severe form of lactase

Molecular and cellular aspects and regulation of intestinal lactase-phlorizin hydrolase.

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Carbohydrates are hydrolyzed in the intestinal lumen by specific enzymes to monosaccharides before transport across the brush border membrane of epithelial cells into the cell interior. The enzymes implicated in the digestion of carbohydrates in the intestinal lumen are membrane-bound glycoproteins

A retrospective study on the association of gastrointestinal symptoms in children with low lactase activity and low activity of other disaccharidases

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Background: Disaccharides such as lactose and sucrose are sugars commonly found in human diet. They are broken down by mucosal disaccharidases in the duodenum. Previous small studies found no associations between gastrointestinal (GI)

Impaired trafficking and subcellular localization of a mutant lactase associated with congenital lactase deficiency.

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OBJECTIVE Congenital lactase deficiency (CLD) is a cause of disaccharide intolerance and malabsorption characterized by watery diarrhea in infants fed breast milk or lactose-containing formulas. The molecular basis of CLD is unknown. Mutations in the coding region of the brush border enzyme lactase

Rotavirus infection impairs intestinal brush-border membrane Na(+)-solute cotransport activities in young rabbits.

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The mechanism of rotavirus diarrhea was investigated by infecting young, specific pathogen-free, New Zealand rabbits with a lapine rotavirus, strain La/RR510. With 4-wk-old animals, virus shedding into the intestinal lumen peaked at 72 h postinfection (hpi), and a mild, watery diarrhea appeared at

Congenital lactose intolerance is triggered by severe mutations on both alleles of the lactase gene.

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BACKGROUND Congenital lactase deficiency (CLD) is a rare severe autosomal recessive disorder, with symptoms like watery diarrhea, meteorism and malnutrition, which start a few days after birth by the onset of nursing. The most common rationales identified for this disorder are missense mutations or

[Basics of intestinal electrolyte transport (author's transl)].

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In the small and large intestine Na and Cl are absorbed via active transport systems, whereas K appears to distribute passively between the lumen and the blood side of the epithelium. Three types of Na influx mechanisms across the luminal cell membrane of the epithelium may be distinguished: 1. In

Procyanidin from black beans (Phaseolus vulgaris) inhibits nutrient and electrolyte absorption in isolated rat ileum and induces secretion of chloride ion.

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Dietary tannins are reported to impair the absorption of nutrients and minerals in whole animals and in semi-isolated intestinal preparations. The present studies investigated the effect of purified procyanidin from black beans (Phaseolus vulgarus) on tissue electrical parameters, isotopic Na+ and

Congenital Lactase Deficiency: Mutations, Functional and Biochemical Implications, and Future Perspectives.

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Congenital lactase deficiency (CLD) is a severe autosomal recessive genetic disorder that affects the functional capacity of the intestinal protein lactase-phlorizin hydrolase (LPH). This disorder is diagnosed already during the first few days of the newborn's life due to the inability to digest

Lactose Intolerance: What Your Breath Can Tell You

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Lactose intolerance has seen recognized as a clinical syndrome characterized by pain, abdominal distention, flatulence, and diarrhea after the consumption of lactose. Lactose is a common disaccharide found in dairy that requires lactase-phlorizin hydrolase (LPH) to break down into glucose and

Compound missense mutations in the sodium/D-glucose cotransporter result in trafficking defects.

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OBJECTIVE Defects in the Na+-dependent glucose transporter (SGLT1) are associated with the disorder glucose-galactose malabsorption, characterized by severe diarrhea. This study focused on a unique proband with glucose-galactose malabsorption who was investigated 30 years ago, and the aims of the

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