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glucosidase/infarci
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[Glycosphingolipid content and beta-galacto- and beta-glucosidase activity of the blood in acute myocardial infarction and postinfarction cardiosclerosis].
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Content of acid and neutral glycosphingolipids was distinctly higher in blood plasma and cells of patients with acute myocardium infarction as compared with healthy persons. In leukocytes of the patients activity of beta-galactosidase, exhibiting pH optimum at pH 3.6, was decreased with simultaneous
Role of protein kinase C in the reduction of infarct size by N-methyl-1-deoxynojirimycin, an alpha-1,6-glucosidase inhibitor.
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Preischaemic treatment with N-methyl-1-deoxynojirimycin (MOR-14), an alpha-1,6-glucosidase inhibitor, attenuates glycogenolysis and lactate accumulation during ischaemia and markedly reduces infarct size in rabbit hearts. In the present study, we have investigated whether protein kinase C (PKC), a
Serum beta-N-acetylglucosaminidase, beta-D-glucosidase, alpha-D-glucosidase, beta-D-fucosidase, alpha-L-fucosidase and beta-D-galactosidase levels in acute viral hepatitis, pancreatitis, myocardial infarction and breast cancer.
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The specific activities of several glycosidases (beta-N-acetylglucosaminidase, beta-D-glucosidase, alpha-D-glucosidase, beta-D-fucosidase, alpha-L-fucosidase and beta-D-galactosidase) were determined in human sera from a control group to 10 normal subjects and in four groups, each of 10 patients,
N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly reduced infarct size in rabbit hearts.
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BACKGROUND
N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, reduces the glycogenolytic rate by inhibiting the alpha-1,6-glucosidase of glycogen-debranching enzyme in the liver, in addition to possessing an antihyperglycemic action by blocking alpha-1,4-glucosidase in the
Acarbose reduces the risk for myocardial infarction in type 2 diabetic patients: meta-analysis of seven long-term studies.
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OBJECTIVE
To assess if treatment with the alpha-glucosidase inhibitor acarbose can reduce cardiovascular events in type 2 diabetic patients.
RESULTS
This meta-analysis included seven randomized, double-blind, placebo-controlled acarbose studies with a minimum treatment duration of 52 weeks. Type 2
Plasma BNP Levels and Diuretics Use as Predictors of Cardiovascular Events in Patients with Myocardial Infarction and Impaired Glucose Tolerance.
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Alpha-glucosidase deficiency and basilar artery aneurysm: report of a sibship.
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Glycogen deposition in vascular smooth muscle has been demonstrated previously in alpha-glucosidase deficiency but has not been clinically significant. Three sons of healthy, nonconsanguineous parents developed progressive proximal muscular weakness secondary to alpha-glucosidase deficiency. Each
Does Treatment of Impaired Glucose Tolerance Improve Cardiovascular Outcomes in Patients with Previous Myocardial Infarction?
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OBJECTIVE
We evaluated the effects of an alpha-glucosidase inhibitor, voglibose, on cardiovascular events in patients with a previous myocardial infarction (MI) and impaired glucose tolerance (IGT).
METHODS
This prospective, randomized, open, blinded-endpoint study was conducted in 112 hospitals and
Arbutin prevents alterations in mitochondrial and lysosomal enzymes in isoproterenol-induced myocardial infarction: An in vivo study
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The present study demonstrated the protective effects of arbutin (ARB) on hyperlipidemia, mitochondrial, and lysosomal membrane damage and on the DNA damage in rats with isoproterenol (ISO)-induced myocardial infarction (MI). Rats were pretreated with ARB (25 and 50 mg/kg body weight (bw)) for 21
Influence of isoproterenol-induced myocardial infarction on certain glycohydrolases and cathepsins in rats.
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The changes in the activities of certain lysosomal hydrolases, viz., beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, beta-glucosidase, alpha-glucosidase, alpha-galactosidase, alpha-mannosidase, cathepsin B, cathepsin D, and collagenolytic cathepsin, in serum and heart of rats
Combination of N-methyl-1-deoxynojirimycin and ischemic preconditioning markedly reduces the size of myocardial infarcts in rabbits.
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N-methyl-1-deoxynojirimycin (NMDN), an a-glucosidase inhibitor, reduces myocardial infarct size by reducing the glycogenolytic rate through inhibition of the alpha-1,6-glucosidase of glycogen-debranching enzyme in the heart, in addition to possessing an antihyperglycemic action by blocking
A novel anti-diabetic drug, miglitol, markedly reduces myocardial infarct size in rabbits.
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1. We examined whether N-hydroxyethyl-1-deoxynojirimycin (miglitol), a new human anti-diabetic drug with effects to inhibit alpha-1, 6-glucosidase glycogen debranching enzyme and reduce the glycogenolytic rate as well as to inhibit alpha-1,4-glucosidase, could reduce infarct size in the rabbit
Acarbose reduces myocardial infarct size by preventing postprandial hyperglycemia and hydroxyl radical production and opening mitochondrial KATP channels in rabbits.
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BACKGROUND
Acarbose, an antidiabetic drug, is an alpha-glucosidase inhibitor that can inhibit glucose absorption in the intestine. A recent large-scale clinical trial, STOP-NIDDM, showed that acarbose reduces the risk of myocardial infarction. We examined whether acarbose reduces myocardial infarct
Combination of miglitol, an anti-diabetic drug, and nicorandil markedly reduces myocardial infarct size through opening the mitochondrial K(ATP) channels in rabbits.
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The anti-diabetic drug miglitol, an alpha-glucosidase inhibitor, which is currently used clinically, reduces myocardial infarct size by reducing the glycogenolytic rate through inhibition of the alpha-1,6-glucosidase of glycogen-debranching enzyme in the heart. Nicorandil, a K(ATP) channel opener
Repetitive postprandial hyperglycemia increases cardiac ischemia/reperfusion injury: prevention by the alpha-glucosidase inhibitor acarbose.
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Protective effects of the alpha-glucosidase inhibitor acarbose have been reported for various diabetic complications. In the STOP-NIDDM study, even patients without overt diabetes, but with impaired glucose tolerance, had a reduction in cardiovascular events when treated with acarbose. Therefore, we
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