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alpha glucosidase/atrofia
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 95 tuloksia
Effect of inhibition of alpha-glucosidase on age-related glucose intolerance and pancreatic atrophy in rats.
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Oral administration of alpha-glucosidase inhibitor reduces postprandial serum glucose and insulin concentrations; thus, alpha-glucosidase inhibitor is used for the treatment of diabetes mellitus worldwide. In our study, we have evaluated the effect of alpha-glucosidase inhibitor, acarbose, on
Effectiveness of acarbose, an alpha-glucosidase inhibitor, in uncontrolled non-obese non-insulin dependent diabetes.
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The effect of acarbose, an alpha-glucosidase inhibitor, on glycaemic control, was compared with placebo in a double-blind, randomised, group comparison study during 16 weeks in 20 non-obese non-insulin dependent diabetic patients in whom sulphonylurea treatment had been withdrawn. There was
Age-related decline in muscle strength and power output in acid 1-4 alpha-glucosidase knockout mice.
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A hallmark of glycogen storage disease type II, caused by defective alpha-glucosidase (AGLU) activity, is a progressive decline in muscle performance. The objective of this study was to determine the relative contribution to this decline in muscle performance of (1) decline in muscle mass; (2)
Recombinant human acid alpha-glucosidase (rhGAA) in adult patients with severe respiratory failure due to Pompe disease.
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Pompe disease is a rare metabolic myopathy caused by lysosomal α-glucosidase deficiency. Pompe disease ranges from a rapidly progressive course when symptoms present in infancy to a more slowly progressive rate when symptoms present in childhood or adulthood. This open-label prospective exploratory
Ability of adeno-associated virus serotype 8-mediated hepatic expression of acid alpha-glucosidase to correct the biochemical and motor function deficits of presymptomatic and symptomatic Pompe mice.
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The availability of a murine model of Pompe disease has enabled an evaluation of the relative merits of various therapeutic paradigms, including gene therapy. We report here that administration of a recombinant adeno-associated virus serotype 8 (AAV8) vector (AAV8/DC190-GAA) encoding human acid
Effects of long-term treatment with alpha-glucosidase inhibitor on the peripheral nerve function and structure in Goto-Kakizaki rats: a genetic model for type 2 diabetes.
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BACKGROUND
Continuous hyperglycemia is implicated in the pathogenesis of chronic diabetic complications. It is not well known, however, how and to what extent the development of neuropathy is inhibited by blood glucose control in subjects with Type 2 diabetes. We investigated therefore the effects
[Two new mutations in the gene that codes for acid alpha-glucosidase in an adolescent with late-onset Pompe disease].
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INTRODUCTION. Glycogen storage disease type II, or Pompe disease, is a lysosomal disease with an autosomal recessive pattern of inheritance. Late-onset Pompe disease is a progressive metabolic myopathy caused by decreased activity of the enzyme acid alpha-glucosidase (GAA), which gives rise to
Kinetic properties of neutral alpha-glucosidase in the atrophic mucosa of self-emptying blind loops of rat jejunum: a microdensitometric study at two different villus sites.
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The in situ kinetic constants of neutral alpha- glucosidase were determined in the atrophic jejunal mucosa of self-emptying blind loops and in corresponding jejunal segments of control rats, using a quantitative histochemical technique. The apparent maximum velosity (Vmax) and km values were
Long-term ingestion of a fermented soybean-derived Touchi-extract with alpha-glucosidase inhibitory activity is safe and effective in humans with borderline and mild type-2 diabetes.
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Water-extracted Touchi, a traditional Chinese food, exerts a strong inhibitory activity against rat intestinal alpha-glucosidase in foodstuffs, and Touchi-extract (TE) has been shown to have an antihyperglycemic effect in rats and humans after a single oral administration. In the present
Combination therapy of alpha-glucosidase inhibitor and a sulfonylurea compound prolongs the duration of good glycemic control.
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The aim of this study was to investigate whether combination therapy of alpha-glucosidase inhibitor and a sulfonylurea (SU) drug can prolong the duration of good glycemic control compared with SU alone in patients with type 2 diabetes. The open prospective study included 124 Japanese patients with
Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding.
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Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight,
Studies targeting α-glucosidase inhibition, antiangiogenic effects, and lipid modification regulation: background, evaluation, and challenges in the development of food ingredients for therapeutic purposes.
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Since the discovery of α-glucosidase inhibitors and their inhibitory effects on the digestion of carbohydrates, promising results have been obtained as to the antidiabetic effects of this family of compounds. Antiangiogenic compounds have been identified that suppress tumor growth via a unique
Role of intestinal peptides and the autonomic nervous system in postprandial hypotension in patients with multiple system atrophy.
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Postprandial hypotension (PPH) is a major clinical problem in patients with autonomic failure such as that observed in multiple system atrophy (MSA). The pathophysiology of PPH remains unclear, although autonomic dysfunction and gastrointestinal vasoactive peptides have been suspected to participate
Metabolic abnormalities in the genetically obese and diabetic Otsuka Long-Evans Tokushima Fatty rat can be prevented and reversed by alpha-glucosidase inhibitor.
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The recently developed Otsuka Long-Evans Tokushima Fatty (OLETF) rat is known to develop insulinopenic diabetes after a prolonged period in a condition resembling non-insulin-dependent diabetes mellitus (NIDDM). We examined the effect of pharmacological intervention with a potent intestinal
Effects of Bay m 1099, an α-Glucosidase Inhibitor, on Starch Degradation in Germinating Mung Beans.
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To examine the mechanism of starch degradation in legume cotyledons and the physiological role of α-glucosidase, mung bean seeds were germinated in the presence of Bay m 1099, an α-glucosidase inhibitor. Bay m 1099 (10 μg/ml medium), which minimized the growth deterioration of the mung bean
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