3Glucose and ketone body kinetics in diabetic ketoacidosis

John M. Miles, John E. Gerich

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


The hyperglycaemia and hyperketonaemia of diabetic ketoacidosis areinitiated primarily by overproduction of these substrates; subsequent maintenance of hyperglycaemia occurs, in large part, due to impaired utilization of glucose, whereas overproduction of ketone bodies continues to be the major mechanism for maintenance of hyperketonaemia. Insulin deficiency results in increased rates of lipolysis and provides increased substrate (free fatty acids) for ketogenesis. Hyperglucagonaemia can augment ketogenesis further in the setting of insulin deficiency. It is likely that other counter-insulin hormones (growth hormone, catecholamines) also contribute to the pathogenesis of DKA, though their role is less well defined. Insulin corrects DKA largely via suppression of lipolysis (and thus ketone body production); insulin suppresses glucose production at lower levels than it does ketone body production.

Original languageEnglish (US)
Pages (from-to)303-319
Number of pages17
JournalClinics in Endocrinology and Metabolism
Issue number2
StatePublished - Jul 1983

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology


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