Brief and Partial Review of Ketosis Physiology

Ketosis Physiology not to be confused with Diabetic Ketoacidosis:

Interrelationship between Malonyl-CoA and Carnitine Palmityl Transferase 1 (CPT-1)



As Liver glycogen drops Malonyl-CoA levels drop, the enzyme CPT-1 becomes active which then transports Free Fatty Acids (FFA) into the mitochondria, which then causes rapid fat oxidation, the by product acetyl-CoA levels rise rapidly, which is typically used for energy production through the Kreb cycle when carbs are available. However, when carbs are unavailable acetyl-CoA accumulates in the liver. High levels of acetyl-CoA are then condensed in the liver, into acetoacetate, which can be further converted into beta-hydroxybutyrate and acetone, the final 2 of the ketone bodies.



As in Diabetic Ketoacidosis, there is a bit of difference in the onset of it. As in ketosis, one of the primary changes that occurs is a lack of insulin (ketosis there is a restriction in dietary carbohydrates that lowers the insulin) (DKA, specifically happens in type I diabetics, there is a lack of insulin possibly due to lack of injection of insulin. Thus causing glucagon levels to be higher, which then signals the liver to convert FFA into ketones, since this ketosis is induced by lack of insulin and not lack of carbs the body is still using carbs as the primary fuel source which in turn doesn't allow the body to adapt to using ketones as a viable fuel source causing the blood to be saturated by ketones and further increasing the acidity of the blood and depreciating the buffering ability of the blood. A non-diabetic persons body has built in feed-back loops that once ketone levels rise too high the body will secrete insulin which will decrease the produce of ketone bodies, then signaling the body to excrete excess ketone bodies through urine. In a type I diabetic this feed-back loop is not functional due to the pancreas' inability to produce insulin, further allowing the body to produce ketones and wreaking havoc on the person. It is typically treated with an insulin injection.