ABSTRACTS

Vanadate mimics insulin action in vitro, lowers blood glucose in diabetic rats, and has been suggested as a novel treatment for diabetes. However, it also inhibits feeding which itself could lower blood glucose. We assessed the contribution of hypophagia to vanadate's anti-hyperglycaemic action in a 3-week study of streptozotocin-diabetic (STZ-DM) rats. Untreated diabetics (n =8) ate significantly more than non-diabetic controls (n=8; food intake, 68±3 (SEM) vs 44±1 g rat⁻¹ day⁻¹, p<0.001). Diabetic rats (n=8) given sodium metavanadate (0.5 mg in 0.5 ml water by gavage twice-daily after diabetes induction) had significantly lower food intakes (41 ±2 g rat⁻¹ day⁻¹, p < 0.001) than untreated diabetics. Vanadate-treated diabetic rats had significantly lower blood glucose levels (average after 5 days, 16.5± 3.0 mmol l⁻¹1) than untreated diabetics (38.2±3.4 mmol l ⁻¹, p < 0.001). However, diabetic rats (n =8), not given vanadate but restricted to the food intake of the vanadate-treated diabetics, showed virtually identical blood glucose falls to 17.8±2.6 mmoll -1 (p<0.05 vs vanadate-treated diabetics). In non-diabetic rats (n = 8), vanadate significantly reduced food intake to 33±1 g rat⁻¹ day⁻¹ (p<0.05 vs untreated non-diabetics) but did not significantly affect blood glucose (7.7±1.1 mmol l⁻¹ vs 9.1 ±0.6 mmol l⁻¹ in untreated non diabetics; p>0.05).\ud\udThe glucose-lowering effect of vanadate in STZ-DM rats is therefore due entirely to its suppression of feeding. It may have no specific anti-diabetic action in vivo