Excessive circulating glucagon levels have been reported in all forms of diabetes, clinical or experimental. The hyperglucagonemia of diabetes results from an excessive secretion of the hormone secondary from a deficit in insulin secretion and/or a dysfunction of various cells within the islets of Langerhans (somatostatin) leading to the notion of "paracrinopathy". Hyperglucagonemia contributes to the fasting and postprandial hyperglycemia in diabetic patients through an increased hepatic glucose production (mainly gluconeogenesis). The aim of the present review is to summarize the clinical and experimental arguments suggesting that glucagon is essential for the development of glucose dysregulation in diabetes.
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