3Glucose and ketone body kinetics in diabetic ketoacidosis

John M. Miles, John E. Gerich

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

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
Volume12
Issue number2
DOIs
StatePublished - 1983
Externally publishedYes

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Ketone Bodies
Diabetic Ketoacidosis
Insulin
Kinetics
Lipolysis
Hyperglycemia
Maintenance
Glucose
Hormones
Substrates
Nonesterified Fatty Acids
Growth Hormone
Catecholamines

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

3Glucose and ketone body kinetics in diabetic ketoacidosis. / Miles, John M.; Gerich, John E.

In: Clinics in Endocrinology and Metabolism, Vol. 12, No. 2, 1983, p. 303-319.

Research output: Contribution to journalArticle

Miles, John M. ; Gerich, John E. / 3Glucose and ketone body kinetics in diabetic ketoacidosis. In: Clinics in Endocrinology and Metabolism. 1983 ; Vol. 12, No. 2. pp. 303-319.
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