Glucagon, in the setting of absolute or relative insulin deficiency, is thought to contribute to the pathogenesis of hyperglycaemia in diabetes, but much of the evidence is extrapolated from short-term studies to the long-term condition. In the present issue of Clinical Science, Li and co-workers report that infusion of glucagon raised fasting plasma glucose concentrations and impaired glucose tolerance over 4 weeks in mice, thus demonstrating a sustained glycaemic effect of hyperglucagonaemia. Nonetheless, compelling evidence that glucagon contributes to the pathogenesis of hyperglycaemia in diabetes awaits long-term selective reduction of glucagon secretion or action in humans.

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