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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 importance of type 2 diabetes is due to its high prevalence, the difficulties in achieving optimal glucose control (financial, time, quality of life) and the high frequency of chronic microvascular and macrovascular complications that add very significantly to the morbidity, mortality and overall cost of the disease. Numerous risk factors have been identified that predict the future onset of type 2 diabetes in individuals and an early stage of the disease (impaired glucose tolerance) can often be identified. Insulin resistance is central to the pathogenesis and is initially compensated by an increased insulin secretion. Over time, insulin secretion progressively fails and diabetes appears. Several approaches have been proposed for the prevention of diabetes. Lifestyle changes (nutritional therapy and physical activity) have been shown to reduce the frequency of diabetes in small studies and are being assessed in the NIH-funded Diabetes Prevention Trial. Metformin, which reduces insulin resistance and hyperinsulinaemia, is being assessed in this same trial. Acarbose, which has been shown to reduce post-prandial insulin secretion and improve insulin resistance, is being assessed in the STOP-NIDDM trial. The ACE inhibitor ramipril has been shown in the HOPE study to reduce the appearance of diabetes by one third when given to patients with vascular disorders and this class of agents has been shown to improve insulin resistance. Another very promising approach is the use of thiazolidinediones (rosiglitazone, pioglitazone) to improve the insulin resistance and possibly preserve the beta cells by reducing the need for increased insulin secretion. These lifestyle changes and medications have been shown to be safe in the treatment of type 2 diabetes. There is a high probability that one of these approaches will be effective in delaying or preventing type 2 diabetes, and prevention may become a clinical reality in the near future.
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PMID:Prevention of type 2 diabetes. 1196 30

This study compared the effects of acarbose plus glibenclamide combination therapy with acarbose or glibenclamide treatment alone on postprandial blood glucose, serum insulin and C-peptide levels, and the tendency to develop hypoglycaemia. A total of 84 patients with Type 2 diabetes (fasting blood glucose: 120-180 mg/dl; postprandial blood glucose: 140-240 mg/dl) was included in this two-centre, double-blind, double-dummy, placebo-controlled study. Patients were randomised to one of 4 treatment groups: acarbose (100 mg); glibenclamide (3.5 mg); acarbose plus glibenclamide; or placebo. Treatment was administered before a standard breakfast, and fasting (07.30 h, 08.00 h) and postprandial (09.00, 10.00, 11.00, 12.00 h) blood glucose, serum insulin and C-peptide levels were determined. Acarbose plus glibenclamide treatment significantly reduced the mean increase in postprandial blood glucose levels (23.7+/-17.3 mg/dl) compared with either acarbose (58.4+/-31.6 mg/dl), glibenclamide (56.9+/-42.8 mg/dl) or placebo (101.6+/-49.2 mg/dl) (p<0.05 for all). Serum insulin levels (mean AUC(7.30-12 h)) observed with acarbose plus glibenclamide combination therapy were significantly lower than those observed with glibenclamide monotherapy (243.5+/-161.1 vs 383.4+/-215.8 hr x microU/ml; p=0.02), and comparable with the values seen with placebo (226.0+/-166.6 hr x microU/ml), suggesting that acarbose modifies the insulin secretion induced by glibenclamide. Glibenclamide monotherapy resulted in a significantly higher rate of decrease in blood glucose level than with acarbose plus glibenclamide (71.8+/-29.9 vs 46.2+/-18.0 mg/dl x h(-1); p=0.0003), and blood glucose levels at 11.00 h were also markedly lower with glibenclamide (84.4+/-29 mg/dl) than acarbose plus glibenclamide (102.0+/-41 mg/dl), suggesting a reduced tendency for hypoglycaemic episodes with acarbose plus glibenclamide than with glibenclamide alone. In all, 6 (29%) hypoglycaemic episodes occurred with glibenclamide, 2 (10%) with acarbose plus glibenclamide and none with acarbose. Acarbose plus glibenclamide combination therapy results in an additive glucose lowering effect and reduced risk for hypoglycaemia. Acarbose modifies the insulin secretion induced by glibenclamide, which explains the lower risk of hypoglycaemia compared with glibenclamide monotherapy.
Diabetes Nutr Metab 2002 Jun
PMID:The effect of combination treatment with acarbose and glibenclamide on postprandial glucose and insulin profiles: additive blood glucose lowering effect and decreased hypoglycaemia. 1217 28

Type 2 diabetes mellitus is a major health problem associated with excess morbidity and mortality. As the prevalence of this metabolic disorder is rapidly increasing and current treatment fails to stabilise the disease in most patients, prevention should be considered as a key objective in the near future. People who develop type 2 diabetes pass through a phase of impaired glucose tolerance (IGT). Defects in the action and/or secretion of insulin are the two major abnormalities leading to development of glucose intolerance. Any intervention in the impaired glucose tolerance phase that reduces resistance to insulin or protects the beta-cells, or both, should prevent or delay progression to diabetes.Acarbose, miglitol and voglibose act by competitively inhibiting the alpha-glucosidases, a group of key intestinal enzymes involved in the digestion of carbohydrates. They decrease both postprandial hyperglycaemia and hyperinsulinaemia, and thereby may improve sensitivity to insulin and release the stress on beta-cells. These compounds do not induce hypoglycaemia and have a good safety profile, although gastrointestinal adverse effects may limit long-term compliance to therapy. The recent placebo-controlled prospective STOP-noninsulin-dependent diabetes mellitus (STOP-NIDDM) trial demonstrated that acarbose 100mg three times daily reduces the risk of developing type 2 diabetes in patients with IGT (relative risk reduction of 25% after a mean follow-up of 3.3 years). The 6-year Early Diabetes Intervention Trial (EDIT), comparing the effect of acarbose 50mg three times daily to that of metformin, showed a trend to a positive effect of acarbose compared with placebo, in a mid-term 3-year analysis, which should be confirmed in the final analysis. To our knowledge, no such prevention intervention trials have been or are currently being performed with miglitol or voglibose. In conclusion, because of its absence of toxicity and its particular mechanism of action on gastrointestinal tract and indirect consequences on both insulin action and beta-cell function, acarbose may be used to prevent type 2 diabetes. If the ongoing EDIT trial confirms the positive results of the recent STOP-NIDDM trial, acarbose could be used, either as an alternative or in addition to changes in lifestyle, to delay development of diabetes in patients with IGT. However, the best dosage of acarbose for this specific indication remains to be specified, especially when all three important parameters, efficacy, tolerance and cost, are taken into consideration.
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PMID:Is there a role for alpha-glucosidase inhibitors in the prevention of type 2 diabetes mellitus? 1269 98

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

This multicentre, double-blind, placebo-controlled study investigated the efficacy of acarbose in Chinese individuals with impaired glucose tolerance (determined using a 75 g oral glucose tolerance test). Subjects were randomised to either placebo or acarbose 50 mg t.i.d. for a period of 16 weeks. Primary efficacy variables were the maximum postprandial plasma glucose value (C(max)) and the serum insulin profile. Secondary efficacy parameters included postprandial glucose profile, maximum postprandial insulin concentration (C(max)), changes in lipid profile and blood pressure and HbA(1c) and body weight and conversion to Type 2 diabetes. In the intention-to-treat analysis, acarbose treatment resulted in significantly higher reductions in postprandial glucose and serum insulin concentrations compared to placebo. Triglyceride concentration was the only lipid parameter to be significantly reduced in acarbose subjects. Loss of body weight was also significantly greater for acarbose than placebo subjects. Some 19 individuals converted to Type 2 diabetes (seven acarbose, 12 placebo), but this difference was not significant. Acarbose is efficacious in improving the metabolic state of individuals with impaired glucose tolerance indicating a potential benefit for the delay or prevention of onset of Type 2 diabetes in Chinese subjects.
Diabetes Res Clin Pract 2003 Sep
PMID:Efficacy of acarbose in Chinese subjects with impaired glucose tolerance. 1296 8

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

Burgeoning obesity is increasing the prevalence of type II diabetes mellitus. As a consequence, there will be an even greater burden of cardiovascular disease, end-stage renal disease, blindness, and lower extremity amputations. If diagnosed, impaired glucose tolerance presents an opportunity for intervention that potentially could delay or prevent the development of diabetes. Recent prospective studies document the effectiveness of exercise and weight reduction in preventing diabetes. Metformin is less effective than intense lifestyle interventions. Acarbose, losartan, orlistat, pravastatin, ramipril, and hormone replacement therapy are associated with lower rates of the development of diabetes. The Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) trial and the Nateglinide and Valsartan in Impaired Glucose Tolerance Outcomes Research (NAVIGATOR) trial were designed to assess not only the prevention of diabetes but also the impact on cardiovascular morbidity and mortality.
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PMID:Preventing type II diabetes mellitus. 1505 49

This double-blind, placebo-controlled single-centre cross-over study assessed the efficacy of acarbose as adjunct to insulin lispro therapy in avoiding postprandial blood glucose rise. A total of 30 type 2 diabetic patients currently treated with insulin were included. On two consecutive days subjects received a standardised breakfast (covered by insulin lispro) and were randomly assigned study medication of either 100 mg acarbose or matching placebo. Basal and prandial insulin doses were maintained during the study period. A total of nine blood samples (for parameter assessment) were taken at 30-minute intervals. Primary efficacy variables were the difference in blood glucose rise from fasting to 90 min after breakfast between acarbose/lispro and lispro monotherapy and the difference in the postprandial glucose profile (area under the curve, 0 - 240 min). Secondary parameters consisted of differences in postprandial C-peptide, insulin and triglyceride time profiles between the two treatments. Acarbose treatment significantly reduced the rise in 90 min postprandial blood glucose (1.95 +/- 1.85 mmol/l) by more than half the increase observed under lispro monotherapy (4.37 +/- 2.13 mmol/l; p = 0.000). Postprandial blood glucose, C-peptide and serum insulin levels (AUC (0 - 240 min)) all significantly improved under acarbose treatment. Triglyceride levels were not affected by the combination therapy. Rapid-acting insulin lispro was efficiently complemented by the different mechanism of action of acarbose resulting in significant improvements of postprandial hyperglycaemia and the insulin profile.
Exp Clin Endocrinol Diabetes 2004 Jun
PMID:The addition of acarbose to insulin lispro reduces acute glycaemic responses in patients with type-2 diabetes. 1521 48

A 57-year-old woman with non-insulin-dependent diabetes mellitus and inadequate glycemic control was prescribed acarbose (100 mg 3 times daily). Two months later she presented with acute hepatitis (ALT 2,300 IU/l). Other causes of liver damage were excluded. Three months after acarbose had been discontinued, all results of laboratory tests returned to normal values. Three years later the patient was given acarbose again. Acarbose (100 mg three times daily) had been added to glibenclamide (15 mg daily) 2 weeks before she presented with acute hepatitis (ALT 2,778 IU/l). Acarbose was stopped and the results of liver tests returned to normal within 2 months. Of the eight cases of acarbose-associated hepatotoxicity previously reported, five (as well as the two presented herein) were Spanish. The latency period, from the start of drug therapy to the onset of liver injury, was relatively long (> 2 months). We suggest that acarbose be included in the list of drugs which may induce acute hepatitis.
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PMID:[Acarbose-induced acute hepatitis. Report of two events in the same patient]. 1532 23


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