Non-insulin-dependent diabetes mellitus is a metabolic disease that is common and is characterized by insulin insufficiency and resistance. Measures such as body weight reduction and exercise improve the metabolic defects, but pharmacological therapy is the most frequently used and successful therapy. The sulphonylureas stimulate insulin secretion. Metformin and troglitazone increase disposal and decrease hepatic glucose output without causing hypoglycemia. Acarbose is a dietary aid that spreads the dietary carbohydrate challenge to endogenous insulin over time. These pharmacological agents, either alone or in combination, can improve blood glucose regulation in patients with non-insulin-dependent diabetes mellitus.

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Pharmacological regulation of blood glucose levels in non-insulin-dependent diabetes mellitus.

Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion.

Acarbose is an inhibitor of intestinal alpha-glucosidase and has been reported to decrease blood glucose concentrations and glycosuria in diabetic patients and animals. In this study we investigated whether this drug could prevent the abnormalities detected in retinal circulation of diabetic rats. Longitudinal paired studies were performed and the changes in retinal circulation were analyzed using video based fluorescein angiography (VFA) methodology in the same animal. Baseline VFA recordings were obtained from 41 rats. These rats were separated into 4 different groups: In group A (n = 12), diabetes was induced by streptozotocin (STZ) injection and the rats were fed with acarbose (40 mg/100 g powdered chow) mixed into regular rat chow; In group B (n = 10), diabetes was induced by STZ injection and the rats were fed with normal chow; In group C (n = 9), the non-diabetic rats were fed with acarbose; In group D (n = 10), the non-diabetic rats were fed with normal chow. At the end of 2 weeks, all rats again underwent VFA recordings. Blood glucose levels and body weights of rats were monitored during the experiment. The mean blood glucose concentration of Group B was raised from 98.5 +/- 8.7 to 342 +/- 30 mg/dl after STZ injection while in Group A, this change in glucose level was partially ameliorated by acarbose (from 102 +/- 15 to 247 +/- 48 mg/dl). In Group C and D, the blood glucose levels were not significantly changed during the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of abnormal retinal hemodynamics in diabetic rats by acarbose, an alpha-glucosidase inhibitor.

Diabetes is characterized by hyperphagia, polydipsia, polyuria, and elevations in blood and urinary glucose. It has also been documented that beta-adrenergic responsiveness is reduced in diabetes. The intestinal glucosidase inhibitor, acarbose (BAY G 5421), decreases postprandial glycemia by delaying carbohydrate absorption. The purpose of this study was to evaluate the effects of chronic acarbose treatment (20 and 40 mg/100 g of diet) on the metabolic and adrenergic parameters altered in streptozotocin (STZ) (50 mg/kg, intravenously [IV] )-induced diabetes. Metabolic parameters were measured daily for 8 weeks. Diabetic rats were hyperphagic, polydipsic, and polyuric within 1 week of STZ treatment. Acarbose treatment did not consistently effect the food intake but did reduce water intake, urinary output, blood glucose, and the urinary loss of glucose associated with STZ-induced diabetes. Adrenergic responses were assessed by monitoring the increase in tail skin temperature (TST) associated with administration of isoproterenol. Diabetic rats were less responsive than controls and acarbose treatment restored responses toward that of the controls. Additionally, 3H-NE release from the tail artery was elevated in the diabetic rat and restored to normal in the acarbose-treated animals. Collectively these data suggest that acarbose treatment is effective in reducing the severity of metabolic and autonomic complications associated with STZ-induced diabetes.

Beneficial effects of dietary acarbose in the streptozotocin-induced diabetic rat.

The dose-dependency of the effects of the α-glucosidase inhibitor Miglitol (BAY m 1099) was investigated in 8 Type II diabetic patients.

H. Vierhapper

Papers

α-GLUCOSIDE HYDROLASE INHIBITION IN DIABETES