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)

alpha-Glucosidase was extracted from a homogenate of human kidney, initially with 0.02 M Tris-HCl buffer, pH 7.6, and subsequently with a mixture of 0.5% cholate and 0.5% Triton X-100 in the same buffer, pH 7.6. The enzyme in each of these two fractions was purified to the electrophoretically pure state by fractional precipitation with ammonium sulfate, column chromatographies on DEAE-cellulose, hydroxyapatite, Bio Gel A-1.5 m and affinity chromatography on heated glutinous rice. The two purified alpha-glucosidase preparations obtained were the same in enzymatic and proteochemical properties, and the molecular weight and isoelectric point estimated were 3 x 10(5) and 4.2, respectively. No evidence for subunit structure was obtained. The optimum pH for activity was 5.6 and the activity was drastically inhibited by Nojirimycin. The alpha-glucosidase readily hydrolyzed maltose, starch, and glycogen, producing only glucose. It hydrolyzed maltotriitol to split the non-reducing end glucose, but scarcely hydrolyzed maltitol or various other heteroglucosides examined. All these proteochemical and enzymatic properties of kidney alpha-glucosidase were the same as those of urine F-1 alpha-glucosidase. Also, kidney tissue alpha-glucosidase produced a clear precipitin line with antisera against urine F-1 alpha-glucosidase. These facts suggest that F-1 alpha-glucosidase in urine originates from kidney tissue.
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PMID:Identity of alpha-glucosidase of human kidney with urine F-1 alpha-glucosidase. 680 53

This study was undertaken to investigate the effect of voglibose, a new alpha-glucosidase inhibitor, on glucose and lipid metabolism in nondiabetic hyperinsulinemic subjects. Sixteen nondiabetic subjects with hyperinsulinemia participated in the study. They were divided into two groups of eight subjects with normal (NGT) and impaired (IGT) glucose tolerance. A meal tolerance test and a 75-g oral glucose tolerance test (OGTT) were performed at the beginning (baseline phase) and end (treatment phase) of the 12-week treatment. Serum lipid levels were measured every 4 weeks throughout the treatment phase and follow-up phase (8 weeks). All patients received 1 0.2-mg tablet of voglibose before each test meal (3 tablets per day). We also measured insulin sensitivity using a steady-state plasma glucose (SSPG) method in eight normotensive hyperinsulinemic subjects and in eight age- and body mass index (BMI)-matched control subjects before and after the drug treatment. Voglibose significantly decreased the responses of plasma glucose and insulin on the meal tolerance test. The area under the curve for 2-hour insulin during the 75-g OGTT decreased after treatment, whereas that for 2-hour glucose did not change before and after treatment. SSPG was reduced after treatment, indicating improvement of insulin sensitivity. Moreover, treatment with voglibose resulted in a significant decline of triglyceride level and an elevation of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-1. These values returned to near-baseline levels after the drug was discontinued. Consequently, we conclude that this agent not only has a direct hypoglycemic effect through decreased absorption of carbohydrate, but also a hypoinsulinemic and hypolipidemic effect via improved insulin sensitivity.
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PMID:Improvement of insulin sensitivity and dyslipidemia with a new alpha-glucosidase inhibitor, voglibose, in nondiabetic hyperinsulinemic subjects. 863 48