What is the role of fasting in the development of alcoholic ketoacidosis (AKA)?

Updated: Aug 27, 2020
  • Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Energy (caloric) restriction secondary to abdominal pain, nausea, or vomiting usually occurs prior to the onset of AKA. [7] Under conditions of starvation, the liver increases the production of ketones from fatty acids to supply the brain, kidney, and other peripheral tissues with a metabolic fuel that can replace glucose. Increased ketogenesis secondary to the utilization of hepatic glycogen stores, with subsequently increased lipolysis and a decreased insulin-to-glucagon ratio, causes starvation ketosis.

Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin. Free fatty acids are removed by the liver, where they primarily undergo oxidation to hydroxybutyric acid and acetoacetate and subsequently are reesterified to triglyceride. Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis.

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