Horm Metab Res 1984; 16(4): 179-182
DOI: 10.1055/s-2007-1014737
© Georg Thieme Verlag, Stuttgart · New York

Effects of an α-Glucosidase Inhibitor, Acarbose, on Blood Glucose and Serum Lipids in Streptozotocin-Induced Diabetic Rats

K. Yamashita, S. Sugawara, I. Sakairi
  • Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken, Japan
Further Information

Publication History

1982

1983

Publication Date:
14 March 2008 (online)

Summary

Effects of either a single dose or a long-term administration of an α-glucosidase inhibitor, acarbose, on blood glucose, cholesterol concentrations in serum lipoprotein fractions, triglycerides and free fatty acids were examined in streptozotocin-induced diabetic rats. In experiment 1, starch loading tests were performed with or without adding acarbose. The addition of acarbose (0.75 mg per kg of body weight or over) significantly reduced the elevation of blood glucose levels.

In experiment 2, the animals were divided into three groups: Group A fed on a control diet. Group B fed on a diet containing 5 mg acarbose in 100 g of diet and Group C fed on a diet containing 20 mg acarbose in 100 g of diet. The food intake in Group C was significantly reduced by 22% as compared to Group A, while the food intake in Group B showed no change.

The high dose of acarbose showed a tendency to lower fasting blood glucose levels, but the difference was statistically insignificant. However, postprandial glucose levels in Group C at each period examined and in Group B at 30 days were significantly lower than the counterparts in Group A.

Acarbose caused a dose-dependent decrease in serum total cholesterol levels and HDL-cholesterol: total cholesterol ratios were elevated in Group B and C. Serum triglyceride levels in Group B and C were extremely lower than those in Group A on and after 20 days.

These results indicate that the addition of acarbose to the diet induces a decrease in postprandial blood glucose levels and simultaneously causes an improvement in lipid metabolism of streptozotocin-induced diabetic rats.

    >