Hyperglycemia and reduced adiposity of streptozotocin-induced diabetic mice are not alleviated by oral benzylamine supplementation

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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Abstract (original English)

Background Benzylamine (Bza) oral administration delays the onset of hyperglycemia in insulin-resistant db -/- mice; a genetic model of obesity and type 2 diabetes. Aim To extend the antihyperglycemic properties of oral benzylamine to a model of insulin-deficient type 1 diabetes. Methods Male Swiss mice were rendered diabetic by streptozotocin treatment (STZ) and divided in two groups: one received 0.5% Bza as drinking solution for 24 d (STZ Bza-drinking) while the other was drinking water ad libitum . Similar groups were constituted in age-matched, nondiabetic mice. Food intake, liquid intake, body weight gain and nonfasting blood glucose levels were followed during treatment. At the end of treatment, fasted glycemia, liver and white adipose tissue (WAT) mass were measured, while glucose uptake assays were performed in adipocytes. Results STZ diabetic mice presented typical features of insulin-deficient diabetes: reduced body mass and increased blood glucose levels. These altered parameters were not normalized in the Bza-drinking group in spite of restored food and water intake. Bza consumption could not reverse the severe fat depot atrophy of STZ diabetic mice. In the nondiabetic mice, no difference was found between control and Bza-drinking mice for any parameter. In isolated adipocytes, hexose uptake was partially activated by 0.1 mmol/L Bza in a manner that was obliterated

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Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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