Glucose and ketone body kinetics in diabetic ketoacidosis.
The hyperglycaemia and hyperketonaemia of diabetic ketoacidosis are initiated 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.
D016883:Diabetic Ketoacidosis / Q000188:drug therapy / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005934:Glucagon; D005947:Glucose / Q000378:metabolism*; D013006:Growth Hormone; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone; D007328:Insulin / Q000627:therapeutic use; D007657:Ketone Bodies / Q000378:metabolism*; D007700:Kinetics; D008657:Metabolic Clearance Rate; D009638:Norepinephrine
D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007657:Ketone Bodies; D013006:Growth Hormone; D006493:Heparin; D005934:Glucagon; D005947:Glucose; D006854:Hydrocortisone; D009638:Norepinephrine