Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was carried out to examine whether the responsiveness of small intestinal epithelial cells to dietary carbohydrate varied during the daily 24 h cycle. The effect of sucrose on disaccharidase activities was compared during a period of decreasing disaccharidase activities, i.e. between 22.00 and 10.00 hours, and increasing disaccharidase activities, i.e. between 10.00 and 22.00 hours, in the jejunum of 7-week-old-rats. Rats were fed on a low-starch, high-fat diet (Lst; starch 5 and fat 73% of gross energy), or a high-starch, low-fat diet (Hst; starch 70 and fat 7% of gross energy). Both dietary groups exhibited typical diurnal variations in jejunal sucrase (EC 3.2.1.48), maltase (EC 3.2.1.20) and lactase (EC 3.2.1.23) activities, exhibiting a peak around 22.00 hours and a trough at approximately 10.00 hours. When rats were fed on diet Lst for 7 d and then force-fed on an isoenergetic sucrose diet (S; sucrose 40 and fat 37% of gross energy) for 6 or 12 h they exhibited increased sucrase, maltase and lactase activities compared with rats fed on diet Lst. The absolute increase in disaccharidase activities was similar regardless of the time diet S was given or whether rats were killed at 10.00 hours or at 22.00 hours. Analyses of sucrase and lactase activities along the villus-crypt columns showed that the distribution of cell cohorts that responded to diet S was not influenced by the time of introduction of diet S. These findings suggest that small intestinal epithelial cells possess the ability to respond to dietary carbohydrate throughout the daily 24 h cycle.
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PMID:Dietary-induced increases of disaccharidase activities in rat jejunum. 159 99

Saccharomyces cerevisiae regulatory genes CAT1 and CAT3 constitute a positive control circuit necessary for derepression of gluconeogenic and disaccharide-utilizing enzymes. Mutations within these genes are epistatic to hxk2 and hex2, which cause defects in glucose repression. cat1 and cat3 mutants are unable to grow in the presence of nonfermentable carbon sources or maltose. Stable gene disruptions were constructed inside these genes, and the resulting growth deficiencies were used for selecting epistatic mutations. The revertants obtained were tested for glucose repression, and those showing altered regulatory properties were further investigated. Most revertants belonged to a single complementation group called cat4. This recessive mutation caused a defect in glucose repression of invertase, maltase, and iso-1-cytochrome c. Additionally, hexokinase activity was increased. Gluconeogenic enzymes are still normally repressible in cat4 mutants. The occurrence of recombination of cat1::HIS3 and cat3::LEU2 with some cat4 alleles allowed significant growth in the presence of ethanol, which could be attributed to a partial derepression of gluconeogenic enzymes. The cat4 complementation group was tested for allelism with hxk2, hex2, cat80, cid1, cyc8, and tup1 mutations, which were previously described as affecting glucose repression. Allelism tests and tetrad analysis clearly proved that the cat4 complementation group is a new class of mutant alleles affecting carbon source-dependent gene expression.
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PMID:Extragenic suppressors of yeast glucose derepression mutants leading to constitutive synthesis of several glucose-repressible enzymes. 200 6