maltase

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maltase

[′mȯl‚tās]
(biochemistry)
An enzyme that catalyzes the conversion of maltose to dextrose.
References in periodicals archive ?
AT-GAA, which is the first ever investigational product for Pompe disease to receive breakthrough designation, consists of ATB200, a unique recombinant human acid alpha-glucosidase (rhGAA) enzyme with optimized carbohydrate structures, particularly mannose-6 phosphate (M6P), to enhance uptake, co-administered with AT2221, a pharmacological chaperone, according to the company.
(5) For dual therapy, metformin should be used plus another agent, in the following order of preference: GLP-1 receptor agonist, SGLT-2 inhibitor, DPP-4 inhibitor, thiazolidinedione, basal insulin, colesevelam (a bile acid sequestrant), bromocriptine (a dopamine-receptor agonist), alpha-glucosidase inhibitor, and, last, sulfonylurea.
Pharmacological agents like metformin, thiazolidinediones and alpha-glucosidase inhibitors have also demonstrated the potential to delay progression to diabetes and may be considered in those individuals with high risk of progression to diabetes and increased cardiovascular risk.
Pompe disease (glycogen storage disease Type II, acid maltase deficiency, and OMIM #232300) is a rare, progressive, autosomal recessive metabolic disorder caused by a deficiency of the lysosomal enzyme acid alpha-glucosidase (GAA).
Voglibose (Basen, AO-128), one of the most important alpha-glucosidase inhibitors.
Mutations in the acid alpha-glucosidase (GAA) gene, located at locus 17q25.3, are responsible for the disease leading to reduced activity of the acid alpha-glucosidase enzyme.
Choudhary, "Inhibition of alpha-glucosidase by oleanolic acid and its synthetic derivatives," Phytochemistry, vol.
Salyers, "Characterization of a neopullulanase and an alpha-glucosidase from Bacteroides thetaiotaomicron 95-1," Journal of Bacteriology, vol.
Pompe disease is an autosomal recessive genetic disorder characterized by deficiency of the enzyme alpha-glucosidase. Onset and phenotypic spectrum of Pompe disease are wide and vary from the early infantile onset (IOPD) (0-1 year) to the late onset form that may present with different phenotypes, ranging from a symptomless to a severe form (LOPED) [1].
* glycosidases (alpha-glucosidase, beta-glucosidase, alpha-mannosidase, N-acetyl-beta-D-glucosidase),