Glucagon and diabetes.
We have considered the evidence, first, that the presence of glucagon is essential in the pathogenesis of the full syndrome that results from complete insulin deficiency; second, that in the diabetic in whom insulin levels are relatively fixed, a rise in glucagon concentration contributes to endogenous hyperglycemia; and, third, that conventional methods of treatment of diabetes do not fully correct either the abnormal glucagon levels or the hyperglycemia, but when insulin therapy is supplemented with somatostatin, an agent which suppresses both glucagon and growth hormone, both hyperglycemia and hyperglucagonemia are corrected. These facts may one day provide a rationale for therapeutic efforts to suppress excess glucagon secretion in the management of diabetes in man.
D000818:Animals; D002908:Chronic Disease; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D005934:Glucagon / Q000097:blood / Q000502:physiology*; D005947:Glucose / Q000096:biosynthesis; D006801:Humans; D007016:Hypophysectomy / Q000009:adverse effects; D007328:Insulin / Q000172:deficiency; D008099:Liver / Q000378:metabolism; D010180:Pancreatectomy / Q000009:adverse effects
D007328:Insulin; D005934:Glucagon; D005947:Glucose