Describe  the molecular mechanism of the development of ketoacidosis.

Ketoacidosis, a metabolic disorder that causes too many ketones in the body due to low insulin levels, is serious. This is when excess fatty acid from stored triglycerides are released to supply energy. It causes an imbalance between energy production and consumption, leading to high levels of ketones.

The body’s key mechanisms that lead to ketoacidosis at a molecular level are outlined below. First , free fatty acids (FFA) are released from adipose tissue into circulation – providing substrates for hepatic & peripheral oxidation – resulting in increased production of acetyl-CoA molecules . Secondly , acetyl-CoA enters mitochondria where it undergoes beta-oxidation leading to further elevation of these molecules & their derivatives (acetoacetate & beta hydroxybutyrate ) . Further metabolism by enzymes such as thiophorase results in decreased citrate concentrations which inhibit ATP synthesis thus limiting glucose uptake/utilization ability while simultaneously promoting glycogenolysis & gluconeogenesis ultimately leading to hyperglycemia & subsequent acidification through generation of H+ ions via lactate dehydrogenase enzyme activity.

In summary , without proper regulation through insulin release there is disruption between glucose regulation & energy availability causing large accumulation of ketone bodies within blood vessels – raising their acidity levels beyond normal range at which point we diagnose someone with ketoacidosis.