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)

Recent studies have demonstrated that the human intestinal enzymes of carbohydrate digestion and metabolism can be regulated by dietary sugars. These studies have utilized direct assay of intestinal mucosal enzyme activity. Mucosa has been obtained by the use of peroral jejunal biopsy techniques which provide 10-15 mg of mucosa in a safe, simple and reproducible manner. Dietary sucrose, as compared to dietary glucose, increases the activities of the jejunal disaccharidases, sucrase and maltase, but not lactase. Fructose reproduces the sucrose effect and appears to be the active principle in the sucrose molecule. Lactose deprivation or lactose feeding does not alter lactase activity. Fructose has been useful in treating one patient with sucrase-isomaltase deficiency. Jejunal glycolytic enzyme activities are also regulated by dietary sugars. Certain enzymes are highest with specific dietary carbohydrates, lower with other sugars and lowest on a carbohydrate-free diet. The regulation of human jejunal glycolytic enzyme activity takes place in hours, whereas the change in disaccharidase activity occurs in 2-5 days. The mechanism of this regulation is not known. Additional investigations have shown that jejunal glycolytic enzyme activities but not the disaccharidases are controlled by oral folic acid as well. This effect occurs within 1 day also. The mechanism is unknown. Large doses of folate have been of benefit in a few patients with certain glycolytic enzyme deficiency states. Preliminary studies have demonstrated that selected patients with chronic undiagnosed intestinal disorders fail to manifest an adaptive response of their jejunal glycolytic enzyme activities to dietary sugars. This condition has been termed a "maladaptation syndrome.".
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PMID:Diet and intestinal enzyme adaptation: implications for gastrointestinal disorders. 16 4

1. Lactose 6'-O-sulphate, N-acetylneuraminyl-(alpha 2 leads to 3)-D-lactose 6'-O-sulphate, N-acetylneuraminyl ?-O-sulphate-(alpha 2 leads to 3)-D-lactose 6'0-O-sulphate, N-acetylneuraminyl ?-O-sulphate-(alpha 2 leads to 6)-D-lactose and N-acetylneuraminyl-(alpha 2 leads to 3)- and -(alpha 2 leads to 6))-lactose 6'-O-sulphate were prepared by chemical sulphation of lactose, N-acetylneuraminyl-lactose and tis isomers by using pyridine-SO3 reagent. 2. Significant kinetic differences were observed in the enzymic hydrolysis of the sulphated derivatives compared with unsubstituted substrates. 3. In the case of reactions catalysed by rat liver lysosomal and Clostridium perfringens neuraminidases (EC 3.2.1.18), the presence of an O-sulphate group in the N-acetylneuraminyl moiety affected the reaction by decreasing the Km and the Vmax, its presence in the galactosyl moiety affected the reaction by decreasing the Km and increasing the Vmax. and its presence in both N-acetylneuraminyl and galactosyl moieties decreased the Km and the Vmax. of the reaction. 4. Mixed-substrate reaction kinetic data indicated competition between the sulphated and unsubstituted substrates for the same active sites on the neuraminidase molecule. 5. Lactose 6'-O-sulphate neither behaved as a substrate nor acted as an inhibitor with respect to unsubstituted lactose and p-nitrophenyl beta-D-galactopyranoside when tested with lactase of suckling rat intestine and Escherichia coli beta-D-galactosidase (EC 3.2.1.23). 6. Preliminary investigation also indicated that, whereas glucose 6-O-sulphate and glucose 3-O-sulphate were were neither substrate nor inhibitor of glucose oxidase (EC 1.1.3.4), galactose 6-O-sulphate was oxidized half as fast as unsubstituted galactose by galactose dehydrogenase (EC 1.1.1.48).
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PMID:Effect of O-sulphate groups in lactose and N-acetylneuraminyl-lactose on their enzymic hydrolysis. 22 64

Lactose tolerance tests were performed on 75 healthy Lebanese volunteers, 12 patients with "Mediterranean lymphoma" and 15 American and West European Caucasians. Small intestinal biopsies were done on 10 intolerant and five tolerant subjects for histological evaluation and lactase assay. Lactose malabsorption was present in 78% of the Lebanese subjects, in all patients with Mediterranean lymphoma and in five of the 15 Caucasians. Two of the five intolerant Caucasians had giardiasis. There was no difference in the prevalence rate among the various Lebanese groups nor among males and females. Symptoms occurred in 91% of the 58 intolerant Lebanese subjects: diarrhea in 71%, abdominal distension in 67%, and cramps in 48%. The increased prevalence of lactose intolerance with Mediterranean lymphoma is probably secondary to the pathological changes in the intestinal mucosa and protein depletion.
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PMID:Lactose intolerance in the Lebanese population and in "Mediterranean lymphoma". 48 18

Lactose tolerance tests are used clinically to screen children and infants. It is assumed that absorption of a lactose challenge in infants would occur in a predictable pattern prior to weaning. Twenty-one infants from 3 to 12 months of age were studied. The maximum blood glucose rise over fasting levels ranged from 11.0 to 62.0 mg/100 ml; the mean was 32.6 mg/100 ml. Six infants had a maximum rise of less than 20 mg/100 ml. Eleven infants (52%) had a maximum rise of greater than 30 mg/100 ml. Signs of intolerance were not noted in any subject. Weight and length were normally disturbed. Results indicate the variance in glucose rise existing within a population of infants growing normally and consuming milk. Gastric emptying, digestion, and absorption may influence the blood glucose rise after a lactose test. Established glucose levels used as an index to lactose absorption in older children and adults may not accurately reflect lactase activity in infants.
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PMID:Blood glucose rise after lactose tolerance testing in infants. 62 43

Lactose tolerance tests (LTT) in 200 normal adult Ceylonese have shown that 145 (72.5%) had a flat LTT, indicating a population prevalence of lactase deficiency of 66.2 to 78.8%. Jejunal lactase estimations in a smaller sample (41) confirmed this. Twelve of 55 subjects (21.8%) with a normal LTT had intestinal symptoms after lactose and intestinal lactase was low in most of them. It is suggested that little lactase is required to elevate the blood sugar but that more may be required to prevent diarrhea. On the other hand, 65.5% had no symptoms despite a flat LTT, and the possible reasons for this are considered.
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PMID:Intestinal lactase deficiency in Ceylon (Sri Lanka). 87 Mar 73

Lactose-tolerance-test (LTT), ethanol-lactose-tolerance-test (ELTT), 14CO2 breath test and 14C-glucose determination were simultaneously performed in 27 healthy subjects, 16 patients with a Billroth II gastrectomy and 6 patients with a malabsorption syndrome. Intestinal mucosal lactase was absent or significant diminished in 5 of the B II cases and in all patients with malabsorption. In the lactase deficient patients a diminished serum glucose rise after ingestion of 50 g lactose was observed in LTT as well as in ELTT. False positive results in LTT could not be prevented by performing the ELTT. Furthermore the ELTT is not suitable for ambulant investigations because of the required high ethanol load of 0.5 g/kg. Most reliable results were obtained by determination of 14C-serum-glucose after oral application of about 15 muCi of 14C lactose. In respect to lactase level neither false positive nor false negative results were observed. For clinical investigations the procedure of isolation and measurement of 14C-glucose is too laborious however. 14CO2-exhalation test cannot be recommended because of many false positive and false negative results. Moreover 14CO2-exhalation seemed to be insensible and predominant depending on factors other than lactose absorption.
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PMID:[Diagnostics of lactose-malabsorption: value of tolerance tests and 14CO2 exhalation test in patients with and without lactase deficiency (author's transl)]. 99 41

Studies have been done on the effect of Penicillin, Streptomycin and Isonicotinic Acid hydrazide on small intestinal oligosaccharidase and it was observed that the drug penicillin inhibited the enzyme lactase and sucrase by 62.7% and 34.7% respectively, whereas I.N.H. inhibited the enzyme sucrase and maltase by 57.1% and 56.14% respectively. Streptomycin did not show any inhibitory effect on those enzymes. Lactose tolerance test showed impairment of lactose absorption in case of penicillin. Fasting serum sugar level was diminished both in penicillin and streptomycin and the absorption capacity was increased after oral administration of streptomycin.
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PMID:Studies on the effect of penicillin, streptomycin and isonicotinic acid hydrazide on small intestinal oligosaccharidase. 115 32

Lactose intolerance is being reported in many populations. Yet, milk is highly nutritious and methods are being explored to use milk while limiting the lactose content. Thirty-two blacks 13-19 years of age were studied to determine a blood sugar rise with 8 ounces of the following test milks: 1) untreated whole milk (12 g/lactose); 2) 90% lactose hydrolyzed milk (1.2 g/lactose); and 3) 50% lactose hydrolyzed milk (6 g/lactose). In the 22 lactose malabsorbers, the peak blood sugars were: 1) untreated whole milk--4.4 mg/100 ml, 2) 90% lactose hydrolyzed milk--14.5 mg/100 ml, and 3) 50% lactose hydrolyzed milk--8.8 mg/100 ml. The 10 blacks with normal lactose absorption had a comparably high peak blood sugar on all three test milks. Differences between the blood sugar in the lactose absorbing and malabsorbing subjects when drinking untreated whole milk are significant (P less than 0.001); so are differences in the lactose malabsorbing subjects consuming untreated whole milk and 90% lactose hydrolyzed milk (P less than 0.001) as well as 50 and 90% lactose hydrolyzed milk. Symptoms were reported by three lactose malabsorbing subjects with untreated whole milk with two of the three symptomatic with 90% lactose hydrolyzed milk and none with 50% lactose hydrolyzed milk. No symptoms were reported by the lactose absorbers. Significant improvement in absorption with 90% lactose hydrolyzed milk is seen in low lactase subjects. Lactose hydrolyzed milk may serve as an important alternative for food planners wanting to provide milk to high risk populations with low lactase levels.
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PMID:Lactose hydrolyzed milk. 117 37

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

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


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