Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We investigated the effect of acarbose, an alpha-glucosidase and pancreatic alpha-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 (r = 0.68, P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.
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PMID:Inhibition of gastric emptying by acarbose is correlated with GLP-1 response and accompanied by CCK release. 1151 88

This study investigated the effects of the alpha-glucosidase inhibitor, acarbose, on glycemic control and insulin secretion in thalassemic patients with impaired glucose tolerance. The safety and tolerability of the drug were also evaluated. Nine patients (4 men and 5 women, aged 20-34 years) with beta-thalassemia major received a standardized nutritional test load prior to and following 3 months treatment with acarbose 100 mg t.i.d. Blood glucose, insulin and C-peptide levels were measured at 0, 60, 90 and 120 min post-loading. Plasma glucose levels after 3 months of acarbose treatment tended to be slightly lower than pre-treatment levels. Although fasting serum insulin and plasma C-peptide levels were unchanged after acarbose therapy, postprandial serum levels of both hormones were markedly reduced (by 24-47% and 19-32%, respectively, at 60-120 min post-loading). Body mass index, liver enzymes and serum lipids were unaltered following acarbose treatment. Gastrointestinal disturbances were mild and tended to decrease during the course of acarbose therapy. Acarbose is a well-tolerated agent for the management of thalassemic patients with glucose intolerance and normal or increased insulin secretion. It is possible that acarbose may prevent or delay progression from impaired glucose homeostasis to frank insulin-dependent diabetes mellitus.
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PMID:Impaired glucose homeostasis in young adult thalassemic patients: a pilot study with acarbose. 1187 86

The alpha-glucosidase inhibitor acarbose is a drug used to treat type II diabetes mellitus. It occasionally causes diarrhea. Acarbose related colitis has been reported. This note explains how such side effects may occur. Because of small intestine alpha-glucosidase inhibition, increased starch reaches the colon. Increased colonic starch allows the flora to generate increased butyrate. Absorbed butyrate causes up-regulation of prostaglandin E series production and the latter generates water and electrolyte loss. A colitis results when this acarbose driven process is extreme. Acarbose should be avoided in pregnancy until above can be disproved due to teratogenic and labor inducing potential of prostaglandin E. A theoretical reason for avoiding acarbose in Crohn's disease is presented. Despite these considerations, acarbose remains a safe medicine and may even have salutary intestinal consequences stemming from the same physiology as outlined here.
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PMID:Acarbose related diarrhea: increased butyrate upregulates prostaglandin E. 1200 1

Several epidemiological studies have shown an association between postprandial hyperglycemia and mortality from cardiovascular disease. Postprandial hyperglycemia is frequently associated with visceral obesity which plays a key role in metabolic abnormalities such as dyslipidemia and hypertension. Inhibitors of alpha-glucosidase and nateglinide have beneficial effects on the metabolic syndrome associated with visceral obesity. Voglibose in combination with diet therapy reduces visceral fat deposition and ameliorates insulin resistance. Acarbose slightly reduces blood pressure of hypertensive diabetic patients. Nateglinide, a rapidly acting insulin secretagogue, lowers postprandial glucose levels without significant body weight gain. These drugs may protect pancreatic beta-cells from postprandial glucose toxicity and prevent the progression of diabetes.
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PMID:[Pharmacological treatment of postprandial hyperglycemia in hypertensive patients with type 2 diabetes mellitus]. 1287 88

Dumping syndrome is a sequel of gastric surgery in adults and Nissen fundoplication in children. The syndrome is characterized by various gastrointestinal symptoms as well as irritability, diaphoresis and lethargy. Shortly after a meal, symptoms are associated with hyperglycemia (early dumping), followed by late dumping symptoms associated with reactive hypoglycemia. Several therapeutic and dietary manipulations failed to control these symptoms in previous reports as well as in an infant we have followed after Nissen fundoplication. Acarbose, an alpha-glucosidase inhibitor, has been used sporadically in adults after gastric surgery, but only once in children. In most of these studies, the effect of acarbose (on reactive hypoglycemia) was evaluated over several hours postprandially or after oral glucose load. In our study, we recorded glucose dynamics by a continuous glucose monitor system over 2 to 3 days before and during acarbose treatment, while the patient was on a well-controlled diet. These measurements (720 before and 832 on therapy) suggested that both early and late dumping symptoms are causally related to the rate of glucose elevation and decline, rather than to glucose peak and nadir, respectively. Acarbose attenuated both postprandial glucose hyperglycemia and reactive hypoglycemia, which subsequently led to a significant reduction in dumping symptoms. In a follow-up of 14 months, acarbose was well tolerated and the frequency of dumping symptoms was remarkably reduced.
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PMID:Acarbose treatment of infant dumping syndrome: extensive study of glucose dynamics and long-term follow-up. 1294 6

Acarbose--the most extensively investigated and widely prescribed alpha-glucosidase inhibitor--reduces postprandial plasma glucose excursions by delaying the absorption of carbohydrate from the small intestine. Acarbose is an effective first-line therapy for patients with newly diagnosed type 2 diabetes, and induces a further improvement in glycemic control when used in combination with other antidiabetes agents. By decreasing postprandial hyperglycemia and improving insulin sensitivity, acarbose therapy also reduces fasting and postprandial serum insulin, fasting plasma glucose, and hemoglobin A1c levels. As the burden of type 2 diabetes continues to grow, there is a great need for an oral antidiabetes agent with a proven ability to prevent the development of micro- and macrovascular complications, and maintain long-term glycemic control. More than 15 years of clinical investigation have confirmed the sustained efficacy, tolerability, and excellent safety profile of acarbose in a wide range of patient types. Furthermore, the results of the recent Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) showed that acarbose therapy significantly decreased the risk of cardiovascular events in high-risk individuals with glucose intolerance. Acarbose is therefore a convenient and effective long-term option for the treatment of type 2 diabetes, with the added benefit of reducing cardiovascular risk.
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PMID:Review of acarbose therapeutic strategies in the long-term treatment and in the prevention of type 2 diabetes. 1470 48

Acarbose (Glucobay; Bayer) is an alpha-glucosidase inhibitor used to treat diabetes and which may have a role in the prevention of type 2 diabetes. The present study investigated the effects of acarbose treatment on the site and extent of starch digestion, large-bowel fermentation and intestinal mucosal cell proliferation. Eighteen young male Wistar rats were fed "Westernised" diets containing 0, 250 and 500 mg acarbose/kg (six rats/diet) for 21 d. For most variables measured, both acarbose doses had similar effects. Acarbose treatment suppressed starch digestion in the small bowel but there was compensatory salvage by bacterial fermentation in the large bowel. This was accompanied by a substantial hypertrophy of small- and large-bowel tissue and a consistent increase in crypt width along the intestine. Caecal total SCFA pool size was increased more than 4-fold, with even bigger increases for butyrate. These changes in butyrate were reflected in increased molar proportions of butyrate in blood from both the portal vein and heart. There was little effect of acarbose administration on crypt-cell proliferation (significant increase for mid-small intestine only). This is strong evidence against the hypothesis that increased fermentation and increased supply of butyrate enhances intestinal mucosal cell proliferation. In conclusion, apart from the increased faecal loss of starch, there was no evidence of adverse effects of acarbose on the aspects of large-bowel function investigated.
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PMID:Starch digestion, large-bowel fermentation and intestinal mucosal cell proliferation in rats treated with the alpha-glucosidase inhibitor acarbose. 1500 21

Numerous individuals complain of malaise attributed to hypoglycaemia. However, the diagnosis of hypoglycaemia is rarely documented and most often overstated. Reactive hypoglycaemia in the postprandial state is rather exceptional. The diagnosis relies upon the measurement of plasma glucose concentration (< 3 mmol/l or 55 mg/dl) at the time of the malaise. Reactive hypoglycaemia is generally associated with adrenergic symptoms and, less often, with cognitive disturbances. Importantly, a plasma glucose concentration below 3 mmol/l during an oral glucose tolerance test is not sufficient to decide that the patient suffers from reactive hypoglycaemia. Treatment is based on dietary advices including frequent small split meals and limitation of carbohydrates with high glycaemic index. Acarbose, a specific inhibitor of gut alpha-glucosidase enzymes, may be helpful in case of diet failure. As compared with true reactive hypoglycaemia, a postprandial hyperadrenergic reaction without real concomitant hypoglycaemia is much more prevalent. Careful anamnesis may suspect such a diagnosis, but other diagnoses such as panic attack or vasovagal reaction should be excluded. Treatment is purely symptomatic and essentially empiric.
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PMID:[Reactive hypoglycaemia, a mysterious, insidious but non dangerous critical phenomenon]. 1518 36

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 investigated the effect of repetitive postprandial hyperglycemia on the cardiac ischemia/reperfusion injury in vivo. Mice were treated daily by single applications of placebo, sucrose (4 g/kg body weight), or sucrose + acarbose (10 mg/kg body weight) by gavage for 7 days. Acarbose treatment significantly reduced the sucrose-induced increase in plasma glucose concentration. Subsequently, animals underwent 30 min of ischemia by coronary artery ligation and 24 h of reperfusion in vivo. In the sucrose group, ischemia/reperfusion damage was significantly increased (infarct/area at risk, placebo vs. sucrose, 38.8+/-7.5% vs. 62.2+/-4.8%, P<0.05). This was prevented by acarbose treatment (infarct/area at risk 30.7+/-7.2%). While myocardial inflammation was similar in all groups, oxidative stress as indicated by a significant increase in lipid peroxides was enhanced in the sucrose, but not in the sucrose + acarbose group. In summary, repetitive postprandial hyperglycemia increases ischemia/reperfusion damage. This effect can be prevented by treatment with the alpha-glucosidase inhibitor acarbose.
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PMID:Repetitive postprandial hyperglycemia increases cardiac ischemia/reperfusion injury: prevention by the alpha-glucosidase inhibitor acarbose. 1567 Nov 53

Acarbose is an antidiabetic drug that inhibits alpha-D-glucosidase and alpha-amylase. We have found discrepancies of serum and urine amylase activities (AA) determined with different assay methods using samples collected from diabetes mellitus patients taking acarbose. As a result of our screening test using the urine samples, we found a 22% probability of discrepancy (the differences between the two methods were > or = 10% at AA > or = 100 U/l). We have measured acarbose in five discrepant samples by high-performance liquid chromatography/mass-spectrometry and quantified very low levels (0.36-0.93 micromol/l) of acarbose in three samples of urine. The inhibition of AA was known not only to be caused by acarbose but also its metabolites. We should suppose that the inhibitory effects of its metabolites on amylase measurements are larger than those of acarbose.
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PMID:[Effects of acarbose on amylase tests]. 1567 40


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