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

Current therapeutic options for the treatment of non-insulin-dependent diabetes mellitus (NIDDM) focus on regimens that primarily lower fasting blood glucose concentrations. In several short-term studies, the alpha-glucosidase inhibitor, acarbose, has been reported to significantly lower post-prandial plasma glucose levels as well as HbA1c. The primary objective of this present study was to assess the long-term efficacy of adjunctive acarbose therapy to improve metabolic control. Over a 1-y period, acarbose or placebo was administered to 4 groups of patients: those managed by diet only, diet and sulfonylurea, diet and biguanide, and diet and insulin. In all treatment groups, the addition of acarbose resulted in significant reductions in postprandial blood glucose levels. Additionally, HbA1C was significantly lower after 12 months of acarbose therapy, compared with placebo, in all groups except the diet and insulin group. The addition of acarbose consequently expands the armamentarium available to clinicians for the optimization of glycemic control in patients with NIDDM.
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PMID:Clinical experience with acarbose: results of a Canadian multicentre study. 854 19

The onset and progression of long-term complications in diabetes mellitus appear to be related to the degree of hyperglycemia and the overall metabolic control. Therefore, an important goal in the therapy of subjects with diabetes is to avoid wide fluctuations in blood glucose concentrations and increases in lipid levels. The first therapeutic maneuver to achieve glycemic control is to establish a correct diet containing complex carbohydrates and an adequate amount of dietary fibers. Dietary fibers are capable of reducing the intestinal uptake of carbohydrates. An additional strategy to reduce the uptake of carbohydrates across the intestine has recently been proposed by Puls et al. This strategy involves the use of inhibitors of alpha-glucosidase, an intestinal enzyme that participates in the breakdown of polysaccharides into disaccharides and monosaccharides. The inhibition of alpha-glucosidase by these agents is competitive and reversible and results in delayed and reduced uptake of carbohydrates across the intestine. This effect attenuates the post-prandial hyperglycemia and subsequent insulin secretory response particularly in subjects with hyperinsulinemia. The compound acarbose is a member of first generation alpha-glucosidase inhibitors. The administration of high doses of acarbose can be associated with side effects such as flatulence, meteorism, abdominal pain, and diarrhea due to the fermentation of non-absorbed carbohydrates in the intestinal lumen. Usually, these effects subside following a few days of therapy and/or reduction of the initial dose. Acarbose has been effectively used to treat type 2 diabetic patients either as a first choice drug or in association with sulfonylurea agents and in type 1 diabetics in association with insulin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[alpha-Glucosidase inhibitors in the therapy of diabetes mellitus]. 856 69

The effects of alpha-glucosidase inhibitor (acarbose) were studied in 36 patients with non-insulin-dependent diabetes mellitus (NIDDM), aged 34-67 years with a mean duration of diabetes of 8.8 +/- 0.9 years. They were poorly controlled with diet plus sulfonylurea alone or plus sulfonylurea combined with metformin drugs. Acarbose, 100 mg three times daily, was additionally given to these patients for six months. Results showed small but significant decreases (P < 0.001) in postprandial blood glucose level. Glycosylated hemoglobin level was lowered significantly (P < 0.001) and was normalised (level of < 8%) in 17 per cent of the patients. Fasting serum triglycerides level decreased significantly (P < 0.01), whereas, no significant changes in serum total cholesterol and HDL cholesterol levels were seen. Body weight also decreased significantly (P < 0.001) at the end of acarbose trial. Flatulence was the major side effect of acarbose found in 42 per cent of the patients but it was well-tolerated and may be transient and self-limited. We concluded that the addition of acarbose to the therapeutic regimens of diet therapy plus sulfonylurea or plus sulfonylurea combined with metformin drugs led to significant improvement of glycemic control. Acarbose may be a safe and valuable adjunct to diet and sulfonylurea and metformin treatments in obese, poorly-controlled patients with NIDDM.
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PMID:Effects of alpha-glucosidase inhibitor (acarbose) combined with sulfonylurea or sulfonylurea and metformin in treatment of non-insulin-dependent diabetes mellitus. 857 67

Non-insulin-dependent diabetes mellitus (NIDDM) is a major health concern for clinicians who are responsible for the care of an aging population. The relationship between hyperglycemia and the chronic complications of retinopathy, nephropathy, and neuropathy has been established in patients with insulin-dependent diabetes mellitus, and it is extremely likely that such a relationship exists in patients with NIDDM as well. Diet and exercise are the cornerstone for the management of NIDDM. The assessment of glycemic control should determine which patients with NIDDM need more aggressive intervention to control hyperglycemia. Pharmacologic treatment options include oral administration of the sulfonylureas, a biguanide, and an alpha-glucosidase inhibitor and subcutaneous administration of insulin. Extensive education about diabetes and self-monitoring of blood glucose levels are important components in maximizing glycemic control. Additional pharmacologic treatment options are necessary when adequate individualized treatment goals are not attained. The goal of therapy is to prevent the onset or progression of long-term microvascular and macrovascular complications. In this review, we present the therapeutic options and outline our approach to the pharmacologic treatment of NIDDM. Relevant medical literature on each treatment modality is reviewed, and the cost of therapy with use of each medication is provided.
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PMID:Pharmacologic treatment options for non-insulin-dependent diabetes mellitus. 900 95

Antiobesity and antidiabetic actions of the alpha-glucosidase inhibitor AO-128 were examined using genetically obese-diabetic rats, Wistar fatty. Ten-week-old, male fatty rats were kept on CE-2 diet containing 10 or 25 ppm of AO-128 for 4 weeks. The average drug intake was calculated to be 0.74 or 1.78 mg/kg/day from the average food intake, respectively. The intestinal maltase and sucrase activities were decreased by AO-128 in a dose-related fashion. Food intake of fatty rats treated with AO-128 was decreased throughout the experiment. This decrease in food intake could hardly be explained only by diarrhea which occurred for the first 5 days of the administration of AO-128. AO-128 normalized hyperglycemia and markedly reduced hypertriglyceridemia and hyperinsulinemia in fatty rats. In addition, AO-128 decreased body weight gain, food efficiency, epididymal adipose tissue weight, carcass weight, and body fat deposition. These findings indicate that AO-128 may be useful for treating human obesity and diabetes.
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PMID:AO-128, alpha-glucosidase inhibitor: antiobesity and antidiabetic actions in genetically obese-diabetic rats, Wistar fatty. 869 66

The biguanide metformin (dimethylbiguanide) is an oral antihyperglycaemic agent widely used in the management of non-insulin-dependent diabetes mellitus (NIDDM). Considerable renewal of interest in this drug has been observed in recent years. Metformin can be determined in biological fluids by various methods, mainly using high performance liquid chromatography, which allows pharmacokinetic studies in healthy volunteers and diabetic patients. Metformin disposition is apparently unaffected by the presence of diabetes and only slightly affected by the use of different oral formulations. Metformin has an absolute oral bioavailability of 40 to 60%, and gastrointestinal absorption is apparently complete within 6 hours of ingestion. An inverse relationship was observed between the dose ingested and the relative absorption with therapeutic doses ranging from 0.5 to 1.5 g, suggesting the involvement of an active, saturable absorption process. Metformin is rapidly distributed following absorption and does not bind to plasma proteins. No metabolites or conjugates of metformin have been identified. The absence of liver metabolism clearly differentiates the pharmacokinetics of metformin from that of other biguanides, such as phenformin. Metformin undergoes renal excretion and has a mean plasma elimination half-life after oral administration of between 4.0 and 8.7 hours. This elimination is prolonged in patients with renal impairment and correlates with creatinine clearance. There are only scarce data on the relationship between plasma metformin concentrations and metabolic effects. Therapeutic levels may be 0.5 to 1.0 mg/L in the fasting state and 1 to 2 mg/L after a meal, but monitoring has little clinical value except when lactic acidosis is suspected or present. Indeed, when lactic acidosis occurs in metformin-treated patients, early determination of the metformin plasma concentration appears to be the best criterion for assessing the involvement of the drug in this acute condition. After confirmation of the diagnosis, treatment should rapidly involve forced diuresis or haemodialysis, both of which favour rapid elimination of the drug. Although serious, lactic acidosis due to metformin is rare and may be minimised by strict adherence to prescribing guidelines and contraindications, particularly the presence of renal failure. Finally, only very few drug interactions have been described with metformin in healthy volunteers. Plasma levels may be reduced by guar gum and alpha-glucosidase inhibitors and increased by cimetidine, but no data are yet available in the diabetic population.
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PMID:Clinical pharmacokinetics of metformin. 874 35

For 10 patients (three women and seven men) with noninsulin-dependent diabetes mellitus, who had been given insulin (22.6 +/- 19.6 U/day) and had frequently shown hypoglycaemia, the insulin dose was slightly reduced and the administration of an alpha-glucosidase inhibitor was simultaneously started. Hypoglycaemic symptoms disappeared immediately and completely, and sugar metabolism immediately before the withdrawal of treatment was not aggravated: the glycosylated haemoglobin level was unchanged and the post-prandial blood glucose level was increased though not significantly. The results of the present study indicate that the combined used of an alpha-glucosidase inhibitor with a reduced insulin dose improves the quality of life of patients and may improve hyperinsulinaemia.
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PMID:Can alpha-glucosidase inhibitors reduce the insulin dosage administered to patients with non-insulin-dependent diabetes mellitus? 874 17

The effects of administration of an alpha-glucosidase inhibitor and a sulphonylurea compound on lipid profile were investigated in patients with non-insulin-dependent diabetes mellitus, (NIDDM) previously treated with sulphonylurea compounds alone, but in whom metabolic control was inadequate. A group of patients (n = 10) were treated with the alpha-glucosidase inhibitor at a dose of 0.2 mg, three times daily, for 4 weeks. Treatment significantly reduced the post-prandial glucose level and the serum total cholesterol level. In addition, there were non-significant reductions in the triglyceride and very low density lipoprotein levels. These preliminary results suggest that administration of alpha-glucosidase inhibitors might improve the lipid profile of patients with NIDDM.
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PMID:Effect of alpha-glucosidase inhibitor in combination with sulphonylurea compounds on lipid profile in patients with non-insulin-dependent diabetes mellitus. 874 18

The effects of treatment with an alpha-glucosidase inhibitor and a reduced dose of sulphonylurea were investigated in patients with non-insulin-dependent diabetes mellitus who had previously been treated with sulphonylurea compounds but who were hypoglycaemic at times. Treatment with a daily dose of 0.6 mg alpha-glucosidase inhibitor and a reduced dose of the previously used sulphonylurea compound for 4 weeks did not significantly affect the glycosylated haemoglobin level. The post-prandial blood-glucose concentration of the patients was unchanged after treatment compared with its value immediately before treatment but differed significantly compared with the value 4 weeks before treatment (P < 0.03); it was considered likely that this change was due to a seasonal increase in calorie intake at the end of the treatment period. Symptoms related to hypoglycaemia disappeared in all of the treated patients.
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PMID:Can alpha-glucosidase inhibitors reduce the dosage of sulphonylurea compounds needed by patients with non-insulin-dependent diabetes mellitus? 874 20

Twenty patients with non-insulin-dependent diabetes mellitus whose glucose metabolism was unsatisfactory, even though they were receiving appropriate dietary therapy, were treated with an alpha-glucosidase inhibitor (0.6 mg/day) for 12 weeks. The connecting peptide immunoreactivity value (selected as the evaluation criterion of post-prandial endogenous insulin secretion) was compared in patients with and without improved glycosylated haemoglobin levels. A significant difference was found between the connecting peptide immunoreactivity value of the group with improved glycosylated haemoglobin levels (5.0 +/- 1.0 ng/ml) and that in the group without the improvement (2.7 +/- 0.9 ng/ml).
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PMID:Insulin secretion levels necessary for efficacy of an alpha-glucosidase inhibitor on glucose metabolism in patients with non-insulin-dependent diabetes mellitus. 874 19


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