Acetone Glucagon

Ketogenesis is an important metabolic function in the liver. It is the result of an increase in lipolysis in the fatty tissue, with a rise in fatty acids. Insulin inhibits ketogenesis, whereas it is accelerated by fasting as well as by glucagons and insulin deficiency. Ketones (acetacetate, 3-hydroxybutyrate, acetone) are synthesized by means of P-oxidation from acetyl-CoA, assuming the production of this substance exceeds the amount required by the hepa-tocytes (and glucose metabolism is simultaneously reduced). The liver itself does not require any ketones acetone is expired, whereas 3-hydroxybutyrate and acetacetate serve as a source of energy. Ketonaemia can lead to metabolic acidosis and electrolyte shifts. 

The glucagon/insulin ratio can rise under certain pathological conditions (i.e., insulin-dependent diabetes). A small percentage of diabetics develop ketoacidosis, a condition that results from the overproduction and underuhlization of ketone bodies. Increased concentrations of p hydmxybutyrate and acetoacetate, which are acids, can cause a drop in the pH of the blood. This acidification, known as acidosis, can impair the ablLity of the heart to contract and result in a loss of consciousness and coma, which, in rare cases, may be fatal. Diabetic ketoacidosis may manifest as abdominal pain, nausea, and vomiting. A subject may hyperventilate (breathe quickly and deeply) to correct acidosis, as described under Sodium, Potassium, and Water in Chapter 10. It is the responsibility of the clinician, when confronted with a subject whose breath smells of acetone or who is hyperventilating, to facilitate prompt treatment. 

D. Decreased insulin levels cause fatty acid synthesis to decrease and glucagon levels to increase. Adipose triacylglycerols are degraded. Fatty acids are converted to ketone bodies in liver a ketoacidosis can occur. There is increased decarboxylation of acetoacetate to form acetone, which causes the odor associated with diabetic ketoacidosis. 

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