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

The ingestion of (14)C-labeled 9,10-dimethyl-1,2-benzanthracene particles, the extracellular release of acid phosphatase, ribonuclease, and alpha-glucosidase, and the egestion of preingested dimethylbenzanthracene particles by Tetrahymena taken from logarithmically growing cultures and resuspended in a dilute salt solution were followed in the presence of several pharmacologic agents. Serotonin, caffeine, and, to a lesser extent, dibutyryl cyclic AMP increased the rate of particle ingestion, but did not alter the rate of release of the three acid hydrolases studied. Added catecholamines did not affect either particle ingestion or acid hydrolase release, but particle ingestion was inhibited by the catecholamine antagonists, dichloroisoproterenol, desmethylimipramine, reserpine, and phenoxybenzamine. These drugs also increased the release of acid phosphatase and ribonuclease in 5-h incubations. Desmethylimipramine acted within 1 h to increase acid hydrolase release, but the effect of dichloroisoproterenol developed more slowly and was secondary to a change in cellular content of the hydrolases. Desmethylimipramine increased the energy of activation for the release of acid phosphatase, while dichloroisoproterenol did not. Both of these drugs enhanced the egestion of preingested dimethylbenzanthracene particles, supporting the view that acid hydrolase release occurs through a cytoproct egestion mechanism. Particle ingestion was also inhibited by colchicine, vinblastine, and cytochalasin B, but these agents had no effect on acid hydrolase release, thus further differentiating the properties of the ingestion mechanism from those of the egestion mechanism. It appears that both microtubules and microfilaments play a role in the ingestion process and that this process may be controlled in part by a cyclic AMP-mediated serotoninergic and adrenergic system.
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PMID:Lysosomal physiology in Tetrahymena. 3. Pharmacological studies on acid hydrolase release and the ingestion and egestion of dimethylbenzanthracene particles. 415 46

As compared to subcutaneous adipocytes, visceral adipocytes have high basal lipolysis, are highly sensitive to catecholamines, and are poorly sensitive to insulin; these traits are amplified when visceral adipocytes hypertrophy. As a result, enlarged visceral fat stores tend to flood the portal circulation with free fatty acids at metabolically inappropriate times when fatty acids are unlikely to be oxidized, thus exposing tissues to excessive free fatty acid levels and giving rise to the insulin resistance syndrome. A logical approach to preventing or correcting visceral obesity is to down-regulate the lipoprotein lipase (LPL) activity of visceral adipocytes relative to that expressed in subcutaneous adipocytes and skeletal muscle. IGF-I activity appears to be a primary determinant of visceral LPL activity in humans; systemic IGF-I activity is decreased when diurnal insulin secretion is low, when hepatocytes detect a relative paucity of certain essential amino acids, and when estrogens are administered orally. The ability of alpha-glucosidase inhibitor therapy to selectively reduce visceral adiposity suggests that down-regulation of diurnal insulin secretion and/or IGF-I activity may indeed have a greater impact on LPL activity in visceral fat than in subcutaneous fat. Thus, low-glycemic-index, vegan, high-protein, or hypocaloric diets can be expected to decrease visceral LPL activity, as can postmenopausal estrogen therapy. Furthermore, estrogen enhances the LPL activity of non-pathogenic gluteofemoral fat cells, whereas testosterone decreases visceral LPL activity in men; this may explain why sex hormone replacement in middle-aged people of both sexes has a favorable impact on visceral fat and insulin sensitivity. Beta-adrenergic activity suppresses transcription of LPL in adipocytes; this phenomenon may contribute to the favorable impact of exercise training on visceral obesity; conceivably, preadministration of safe drugs that boost catecholamine activity (caffeine, yohimbine) could potentiate this beneficial effect of exercise. Glucocorticoids selectively increase the LPL activity of visceral adipocytes; while there is currently no convincing evidence that psychological stress is a major determinant of visceral adiposity, or that stress management techniques can help to correct visceral obesity, reports that anxiolytic therapy can improve glycemic control in type 2 diabetes should encourage further research along these lines.
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PMID:Modulation of adipocyte lipoprotein lipase expression as a strategy for preventing or treating visceral obesity. 1146 Nov 72

The water extraction and composition of pu-erh tea, as well as the hypoglycemic effect of the water extract of pu-erh tea (WEPT) in vivo and in vitro, are reported to investigate its hypoglycemic effect on diabetes. High-performance liquid chromatography and colorimetric methods are used to analyze the tea catechins, caffeine, polyphenols, amino acids, and polysaccharides of the WEPT. The effect of the WEPT on glucose uptake by cultured HepG2 cells and the inhibition effect of rat intestinal sucrase, maltase, and porcine pancreatic amylase are determined in vitro. Then, the blood glucose and insulin levels of intragastrically administered WEPT on fasting and oral glucose tolerance test (OGTT) using type 2 diabetic db/db (BKS.Cg-m +/+ Lepr(db)/J) mice are determined in vivo. The results showed that the WEPT dose-dependently and significantly increased glucose uptake by HepG2 cells and inhibited rat intestinal sucrase, maltase, and porcine pancreatic amylase activity. The WEPT intragastrically given for 4 weeks suppressed the increase in blood insulin and glucose levels of db/db mice fasted overnight. In OGTT, the WEPT improved impaired glucose tolerance and ameliorated retarded insulin response at 60 and 120 min in db/db mice. These results suggest that the WEPT has beneficial effects on glucose homeostasis in type 2 diabetes and in amendment of insulin resistance.
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PMID:Hypoglycemic effect of the water extract of Pu-erh tea. 2295 68