(27-07-15) Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover

The hormone glucagon has long been dismissed as a minor contributor to metabolic disease. Here we propose that glucagon excess, rather than insulin deficiency, is the sine qua non of diabetes. We base this on the following evidence: (a) glucagon increases hepatic glucose and ketone production, catabolic features present in insulin deficiency; (b) hyperglucagonemia is present in every form of poorly controlled diabetes; (c) the glucagon suppressors leptin and somatostatin suppress all catabolic manifestations of diabetes during total insulin deficiency; (d) total â cell destruction in glucagon receptor–null mice does not cause diabetes; and (e) perfusion of normal pancreas with anti-insulin serum causes marked hyperglucagonemia. From this and other evidence, we conclude that glucose-responsive â cells normally regulate juxtaposed á cells and that without intraislet insulin, unregulated á cells hypersecrete glucagon, which directly causes the symptoms of diabetes. This indicates that glucagon suppression or inactivation may provide therapeutic advantages over insulin monotherapy.

Source: J Clin Invest. 2012 Jan 3; 122(1): 4–12. 
Published online 2012 Jan 3. doi:  10.1172/JCI60016 PMCID: PMC3248306

 

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