The hormones involved in intermediary metabolism, exclusive of insulin, that can participate in the development of diabetic ketoacidosis (DKA) are epinephrine, glucagon, cortisol, growth hormone. Describe how they participate in the development of DKA.

The most important concept is that DKA is caused by insulin deficiency and an increase in counterregulatory hormones that include glucagon, catecholamines, cortisol, and growth hormone. These counter regulatory hormones normally antagonize insulin buy increasing glucose production and decreasing tissue use of glucose. Insulin deficiency results in decreased glucose uptake, increased fat mobilization with release of fatty acids and accelerated gluconeogenesis, glycogenesis, and ketogenesis. In the absence of insulin, the release of free fatty acids from adipocytes increases production of ketone bodies by the mitochondria of the liver that exceeds peripheral use. Accumulation of ketone bodies causes a drop in pH and triggers the buffering system associated with metabolic acidosis. Hyperketonemia may result from impaired use of ketones by peripheral tissue, which permits strong organic acids to circulate freely. Bicarbonate buffering then does not occur and the individual develops a metabolic acidosis.