Inhibiting or antagonizing glucagon: making progress in diabetes care.

摘要: Absolute or relative hyperglucagonaemia has been recognized for years in all experimental clinical forms of diabetes. It suggested that excess secretion glucagon by the islet α cells is a direct consequence intra-islet insulin secretory defects. Recent studies have shown knockout receptor administration monoclonal specific antibody make insulin-deficient type 1 diabetic rodents thrive without insulin. These observations suggest plays an essential role pathophysiology diabetes and targeting cell are innovative approaches management Despite active research identification promising compounds, no one selective antagonist presently used treatment Interestingly, besides insulin, several drugs today appear to exert their effects, part, inhibiting (glucagon-like peptide-1 agonists, dipeptidyl peptidase-4 inhibitors, α-glucosidase inhibitors and, possibly, sulphonylureas) action (metformin). The potential risks associated with total suppression include α-cell hyperplasia, increased mass pancreas, susceptibility hepatosteatosis hepatocellular injury risk hypoglycaemia, these should be considered search development new compounds reducing signalling. More than 40 years after its initial description, can longer ignored minimized, correction represents attractive way improve management.