Glucagon and diabetes. I. The failure of hyperglucagonaemia to influence the response of established diabetic ketoacidosis to therapy.
Clinical and biochemical variables were examined during two standardized, low-dose insulin regimens in seven subjects with diabetic ketoacidosis and one with hyperosmolar coma, in order to determine whether glucagon levels can be suppressed in ketoacidosis and whether hyperglucagonaemia influences the clinical and biochemical responses to treatment. Glucagon concentrations were significantly elevated (36.6-697.0 pmol/l) at presentation in all subjects. After institution of insulin treatment (4-8 u/h), glucose and glucagon levels decreased rapidly, and in five of the eight subjects glucagon levels reached undetectable concentrations (less than 3.0 pmol/l) during the initial treatment period. Further, neither plasma glucagon concentrations at presentation, nor the rate of glucagon decline during insulin treatment, appeared to influence the rapidity of the glucose decline or the persistence of the ketoacidosis. Thus, low-dose exogenous insulin suppresses glucagon secretion in diabetic ketoacidosis, and the changes in glucagon concentrations during treatment are unrelated to the clinical response.
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D016883:Diabetic Ketoacidosis / Q000097:blood / Q000188:drug therapy*; D005260:Female; D005934:Glucagon / Q000097:blood*; D006801:Humans; D007328:Insulin / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged
D001786:Blood Glucose; D007328:Insulin; D005934:Glucagon