Reduction of carbohydrate-induced hypertriglyceridemia in (fa,fa) “Zucker” rats by the α-glucosidase inhibitor acarbose (BAY g 5421)

Inhibition of carbohydrate digestion by the α-glucosidase inhibitor acarbose (BAY g 5421) reduces carbohydrate-induced postprandial blood glucose increase and insulin secretion. As a consequence, in feeding experiments sucrose-induced hyperinsulinemia and hypertriglyceridemia in genetically obese (fa,fa) “Zucker” rats were dose-dependently reduced by addition of acarbose to the diet (15–80 mg/100 g feed). The body weight gain was dose-dependently reduced. In short-term experiments with a fat-free diet acarbose not only prevented serum triglyceride and free fatty acid increase in spite of lowered insulin concentrations but also decreased their concentrations below the values obtained on standard feed. Under these conditions there were no significant effects on body weight. Hypertriglyceridemia induced by i.v. injection of the lipoprotein lipase inhibitor Triton WR 1339 was reduced without affecting body weight in “Zucker” rats after 3 days on a fat-free diet supplemented with acarbose. The triglyceride increase was even lower than in animals kept on standard feed. The data demonstrate that acarbose reduces sucrose-induced hypertriglyceridemia in (fa,fa) “Zucker” rats by diminishing VLDL production and/or secretion rather than by increasing VLDL removal from the blood.