Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About 90% of the protein of hamster intestinal brush borders was solubilised in 0.25% (w/v) sodium dodecyl sulphate without total loss of biological activity. Detergent-polyacrylamide gel electrophoresis of the solubilised proteins separated 10-15 bands and partially resolved maltase, lactase, sucrase-maltase, trehalase and alkaline phosphatase activities. The disaccharidases, which were associated with the higher molecular weight proteins, were preferentially solubilised with 0.1%. (w/v) Triton X-100, butanol or papain, whereas Tris and NaI extracted only the lower molecular weight proteins, possible derived from the core filaments. Electrophoresis of brush border proteins metabolically labelled with [14-C] glucosamine suggested that many of the membrane-bound enzymes are glycoproteins. However, chromatography of a papain digest on Sephadex G-200 showed that the sucrase-maltase complex can be separated nearly free of carbohydrate without total loss of activity. The importance of characterizing membrane proteins solubilised by a number of techniques is discussed.
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PMID:Solubilization of brush borders of hamster small intestine and fractionation of some of the components. 113 70

Feeding sodium deoxycholate orally to rats for four days caused depression of the activity of the small intestinal enzymes lactase, sucrase, maltase, alkaline phosphatase, and N-acetyl-beta-glucosaminidase. The first four are brush border enzymes, the last a lysosomal enzyme. Alkaline phosphatase activity recovered very rapidly and rebounded to above the normal level within 24 hours. The activity of the three disaccharidases returned to normal within seven days while no recovery was observed within 96 hours of the activity of the lysosomal enzyme, N-acetyl-beta-glucosaminidase, after removing the bile salt from the diet.
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PMID:Deoxycholate depresses small-intestinal enzyme activity. 114 Jun 27

The objective of this study was to prepare shelf-stable electrolyte beverages from milk permeate. The average composition of permeate was 4.59% total solids and .40% ash. Lactose was hydrolyzed (approximately 80%) with a commercial fungal lactase enzyme. Additional sweetness was provided by sucrose. The pH was reduced to 3.5 to 3.8 by the addition of citric acid. Shelf-stable products were made using four processes: 1) UHT followed by aseptic filling, 2) heating of filled bottles to 85 degrees C for 30 min, 3) addition of .05% benzoate, and 4) nanopore filtration. The mineral composition of the finished product, expressed in parts per million, was calcium, 150; phosphorus, 157; magnesium, 43; potassium, 1166; sodium, 286; iron, 17; copper, 8; and zinc, 3.4. Listeria monocytogenes, Salmonella dublin, Salmonella typhimurium, Escherichia coli, Staphylococcus aureus, and Streptococcus agalactiae grew well when they were inoculated into unacidified, hydrolyzed permeate. None of these organisms were isolated from properly processed products. A shelf-stable electrolyte beverage high in minerals was made from whole milk permeate. This beverage could be used to replace electrolytes lost from the human body. The production of a permeate beverage would help alleviate disposal problems of permeate.
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PMID:Production of an electrolyte beverage from milk permeate. 145 42

UNICEF promotes the use of a very effective, inexpensive treatment of dehydration in developing countries: oral rehydration therapy (ORT), which is oral administration of a solution with equimolar concentrations of sodium and glucose (osmolality of about 300 mosmol). The solution is isotonic with respect to total body water when it reaches the small intestine. It expands the extracellular fluid without changing serum osmolality, thus, brain edema does not occur. Further, metabolic degradation of glucose eventually releases free water. On the other hand, intravenous rehydration with saline solution can be lethal, causing excess free water to expand shrunken cells and, thereby, causing brain swelling, rupture of blood vessels and hemorrhage. Yet, physicians and other health workers in developed countries have been quite sow to accept ORT. Leading conditions of dehydration include insensible loss of water and heat through evaporation from the respiratory tract and skin (common in dry air, hot environment, and fever), sensible loss of water and heat through perspiration (common in hot, humid environment and with warm and absorbent clothing), and irritation of the intestinal mucosa by allergies, infections, toxins, and intolerance to some nutrients, resulting in diarrhea. Diarrhea is indeed the main cause of dehydration. Other causes of dehydration are: failure of the hypothalamus to secrete antidiuretic hormone (ADH), kidney unresponsiveness to ADH, diabetes mellitus, protein-rich nutrition, catabolic states, and brush-border lactase after weaning. Physiological changes in dehydration consist of rigidity of the connective tissue (vascular system and lungs) and intracellular fluid loss to the extracellular spaces, resulting in dry mucous membranes, shrunken muscle cells in the lips and the tongue, soft eyes, and adverse effects to the central nervous system. Children become dehydrated more readily than adults, but they tolerate it better.
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PMID:Water: mechanism of oral rehydration, water deficiency = deficiency in salt. 150 31

Parietal measurements of pH values in patients with various intestinal diseases and in normal subjects have revealed that alkaline medium with gradual elevation of the values in the caudal direction is characteristics of the normal large intestine; acid pH values were registered in patients with lactase insufficiency, nonspecific ulcerative colitis, in contrast to those with post-dysentery colitis and tumors of the large intestine. Lactulose and sodium sulfate were found the factors that significantly influence the large intestine parietal pH values, the effects of wheat bran were lower; magnesium sulfate and sodium hydrocarbonate mineral water with medium mineral content had no effect on parietal pH values.
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PMID:[The use of parietal pH-metry in the diagnosis of intestinal diseases]. 170 48

Oral administration of the antiulcerogenic drug, cimetidine, was studied on kidney-bound hydrolytic enzymes at three different dose levels (30 mg, 100 mg, and 2000 mg/kg body weight) and for single administration for 2 and 24 h, and daily administration for 15 days in mice. It significantly inhibited Na+, K(+)-ATPase, Mg(2+)-ATPase, and Ca2+, Mg(2+)-ATPase in the isolated basolateral membrane (BLM). Brush-border-membrane-(BBM)-associated enzymes, sucrase, lactase, maltase, leucine aminopeptidase, and alkaline phosphatase also showed a marked reduction. Substrate saturation kinetics revealed the nature of inhibition was of mixed type in the case of sucrase, lactase, maltase, and alkaline phosphatase (Km was increased, while Vmax decreased), whereas it was of non-competitive type for leucine aminopeptidase (Km was unchanged, while Vmax decreased). In vitro addition of cimetidine (5-20 mM) to the BBM also inhibited the enzyme activity. Dixon plot produced the inhibition constant (Ki) for cimetidine in the case of maltase, alkaline phosphatase, and leucine aminopeptidase in the order of 14.83, 32.83 and 11.5 mM, respectively. Analysis of lipids revealed a significant reduction in BBM-associated phospholipid and phospholipid/cholesterol molar ratio, while the neutral lipid fraction, i.e., cholesterol and triglycerides were not altered. Free fatty acid exhibited an increase after drug treatment, which was significant at higher dose after 24 h of single and 15 days of daily treatment. BLM-associated lipids did not exhibit any significant change. Cimetidine-induced depression in renal BLM- and BBM-associated disaccharidases and ATPases, at least at the higher dose level, may have serious consequences in the absorption of end-product nutrients.
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PMID:Depression of membrane-bound hydrolases by cimetidine in mouse renal basolateral and brush border. 183 34

Rotavirus enteritis is the leading cause of diarrhea in infants worldwide. A research priority of the World Health Organization is to develop oral rehydration solutions containing amino acids or other additives that will stimulate intestinal absorption more efficiently than the current glucose-based oral rehydration solutions. Glutamine is the principal metabolic fuel of the small bowel and a putative stimulator of mucosal repair. This report describes the transport response to mucosal L-glutamine following intestinal injury caused by porcine rotavirus. Peak symptoms and mucosal damage were observed 2-7 days after oral rotavirus inoculation. In vitro transport studies of the maximally injured region, the midjejunum (80% reduction in lactase), surprisingly, showed transport responses to L-glutamine (30 mmol/L) and L-alanine (30 mmol/L) that were similar qualitatively and quantitatively to those observed in control tissue. Subsequent application of mucosal D-glucose (30 mmol/L) caused additional stimulation of electrogenic Na+ transport, but the response to glucose was blunted (P less than 0.05) in the infected tissues. Glutamine and alanine enhanced Na+ absorption to a similar degree (2-2.5 muEq.cm-2.h-1), but glutamine stimulated equal amounts of electrogenic and electroneutral NaCl absorption, whereas alanine had no significant effect on net Cl- flux. Glutamine is a potentially useful substrate for investigation in oral rehydration solutions for infant diarrhea.
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PMID:L-glutamine stimulates jejunal sodium and chloride absorption in pig rotavirus enteritis. 188 9

1. The metabolic consequences of chronic ethanol feeding was investigated by assay of urinary metabolites. Male Wistar rats were fed a liquid diet containing 35% of total energy as ethanol or isovolumetric, isocaloric and isonitrogenous amounts of the same diet in which ethanol was substituted by isocaloric glucose (controls). 2. At 6 weeks the entire skeletal muscle mass was reduced by approximately 20%. The urinary excretion of nitrogen, urea and uric acid increased by between 23 and 128%. Urinary creatinine excretion was not significantly altered. 3. Urinary excretion of magnesium was significantly increased by 43%. Urinary excretion of sodium, potassium, calcium and phosphate was increased slightly (i.e. 5-22%), but this change was not statistically significant. 4. Proton n.m.r. spectroscopic analysis showed that ethanol feeding reduced the urinary excretion of citrate and 2-oxoglutarate (by approximately 50%), suggesting decreased citric acid cycle activity. There was an increased excretion of alanine (44%), but excretion of succinate and acetate was not significantly altered. Ethanol in the urine of ethanol-fed rats comprised approximately 2% of total ethanol intake and less than 1% of total energy intake. 5. Lactose was detectable in urine of ethanol-fed rats, but not in control rats, reflecting the reported decreased intestinal lactase activity and increased gut permeability in alcoholics. Urinary galactose excretion decreased by 41%, but relatively large increases in lactate excretion (50%) did not achieve statistical significance. 6. It was concluded that chronic ethanol feeding causes disturbances in whole-body nitrogen homoeostasis and alterations in intermediary metabolism.
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PMID:Urinary excretion of nitrogenous and non-nitrogenous compounds in the chronic ethanol-fed rat. 185 Oct 76

During the third week of postnatal life, dramatic ontogenic changes occur in the morphology and enzymology of the small intestine of the infant rat, enabling the animal to make the transition from milk to solid food. To investigate the roles of T4 and GH in regulation of these changes, infant rats were hypophysectomized on day 6 of life by the transauricular technique. Hypophysectomy resulted in diminution of somatic and intestinal growth as well as abnormal maturation of the disaccharidases lactase, sucrase, and maltase when measured on day 25. Administration of either T4 or GH to hypophysectomized animals resulted in moderately increased intestinal growth, while complete restoration of small intestinal growth resulted from administration of the combination of both hormones. Although T4, GH, or the combination of hormones reduced lactase activities, T4 alone produced normal maturation of sucrase and maltase. Neither hypophysectomy nor hormone replacement affected aminooligopeptidase. The molecular structure of lactase, analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was not altered to a major degree in hypophysectomized animals or animals that received hormone replacement, but minor alterations were evident in sucrase structure in hypophysectomy. These studies indicate that 1) T4 and GH actively participate in postnatal regulation of small intestinal ontogeny; 2) thyroid hormones act directly on developing intestinal tissues to independently produce the normal maturation of the disaccharidases by mechanisms that are not likely to involve alterations in processing of the enzyme-protein; and 3) maturation of aminooligopeptidase is not regulated by pituitary hormones, in distinct contrast to the disaccharidases.
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PMID:Pituitary regulation of postnatal small intestinal ontogeny in the rat: differential regulation of digestive hydrolase maturation by thyroxine and growth hormone. 187 80

Age-specific changes in glycosylation of rat intestinal lactase-phlorizin hydrolase were analyzed using enzyme immunoprecipitated from microvillus membranes of suckling, weaning, and adult rats, and carbohydrate moieties were examined by lectin affinity binding, metabolic labeling, and neuraminidase treatment. Lectin binding indicated the presence of N-linked and O-linked oligosaccharide chains containing mannose and galactose throughout development. An age-dependent shift in sialic acid and fucose was seen during the period of weaning; no fucose was detectable in lactase-phlorizin hydrolase until after the rats were 20 days of age, whereas sialic acid was reduced in adult lactase-phlorizin hydrolase. The presence of sialic acid in suckling intestines and fucose in adult was confirmed by metabolic labeling with appropriate radioactive precursors. Sodium dodecyl phosphate-polyacrylamide gel electrophoresis analysis of immunoprecipitated lactase-phlorizin hydrolase from the proximal and mid small intestine showed two bands of approximately 220 and 130 kilodaltons in all age groups. In the distal part of the adult small intestine, lactase-phlorizin hydrolase appeared as two bands of similar size to those found in the proximal and mid portions. In contrast, during the suckling and weaning periods, these distal bands were approximately 225 and 135 kilodaltons. [35S]-methionine labeling and fluorography of neonatal intestines confirmed these observations. The size difference between proximal and distal small intestines was virtually eliminated by neuraminidase treatment. These data indicate that the core structure of microvillus membrane lactase-phlorizin hydrolase, consisting of both N-linked and O-linked oligosaccharides, remains constant during development, although terminal sugars shift from predominantly sialic acid during the suckling period to fucose in adulthood. This alteration in glycosylation of the protein occurs in a different pattern from the postweaning decline in lactase specific activity. Consequently, age-dependent changes in glycosylation cannot account for the decrease in lactase-phlorizin hydrolase-specific activity observed during development.
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PMID:Glycosylation of lactase-phlorizin hydrolase in rat small intestine during development. 210 55


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