Ketogenic amino acids serve important roles in the human body, leading to the study of ketogenic amino acid rich (KAAR) diets as possible treatment for
non-alcoholic fatty liver disease (NAFLD) and
diabetes. Dietary studies of fatty liver disease in mice show that decreasing the intake of ketogenic amino acids lysine and threonine may induce
hepatic steatosis, a major cause of non-alcoholic fatty liver disease. Leucine in particular has been shown to serve an important role in the metabolic pathway for insulin via activation of the
rapamycin complex 1 (mTORC1) and
protein S6 kinase 1 (S6K1) for which over-activation leads to
insulin resistance. Further studies illustrate that ketogenic amino acid rich diets may aid in decreasing obesity and insulin resistance, but their usage remains disputed. Ketogenic diets are shown to alleviate diffuse axonal injury (DAI). This was tested using rats being fed a standard diet in comparison to rats being fed a ketogenic diet post DAI. Rats that were fed a standard diet showed a progressive degradation of myelin, on day 14 post DAI it was evident that myelin sheaths have collapsed, dissolved or disappeared from the injured axons. For the axons with remaining myelin, the myelin was becoming thinner. Rats that were served ketogenic diets presented axons with thicker myelin in comparison to the standard diet rats. The marker that was used to determine axonal injury in this study was
amyloid precursor protein (APP). Rats that were fed a standard diet and an uptake of APP, leading to an increase in damaged/injured axons. == See also ==