in the hepatocytes undergoes gluconeogenesis to form glucose, which can then enter the bloodstream and be shuttled to the skeletal muscle tissue, thus providing it with the energy source it needs. Function The Cahill cycle ultimately serves as a method of ridding the muscle tissue of the toxic ammonium ion, as well as indirectly providing glucose to energy-deprived muscle tissue. Under long periods of fasting, skeletal muscle can be degraded for use as an energy source to supplement the glucose being produced from the breakdown of glycogen. The breakdown of branch chain amino acids yields a carbon skeleton utilized for energy purposes, as well as free ammonium ions. However, its presence and physiological significance in non-mammalian land vertebrates is unclear. For example although some fish use alanine as a nitrogen carrier, the cycle is unlikely to take place due to a slower glucose turnover rate and lower release of alanine from exercising muscle tissue. The alanine cycle also serves other purposes, such as the recycling of carbon skeletons in skeletal muscle and the liver, and participation in the transport of ammonium to the liver and conversion into urea. Studies have demonstrated that the glucose-alanine cycle may play a direct role in regulation of hepatic (liver) mitochondrial oxidation, particularly during periods of extended fasting. Hepatic mitochondrial oxidation is a key process in the metabolism of glucose and fatty acids, involving the Citric Acid Cycle and oxidative phosphorylation, for the generation of ATP. Understanding the factors that influence hepatic mitochondrial oxidation are of great interest due to its function in mediating diseases such as Non-Alcoholic Fatty Liver Disease (NAFLD), Non-Alcoholic steatohepatitis (NASH), and Type 2 Diabetes. A current active area of research is attempting to exploit the regulatory role of hepatic mitochondrial oxidation for the purpose of developing both targeted and non targeted therapeutics for such diseases. The glucose-alanine cycle may be one of these key factors. A study performed on both rodents and humans showed that decreased alanine turnover during a 60 hour period of fasting did correlate with a notable reduction in hepatic mitochondrial oxidation, as compared to subjects who underwent a 12 hour overnight fast. The rate of oxidative activity was quantified primarily by monitoring rates of Citrate Synthase flux (VCS ), a critical enzyme in the process of mitochondrial oxidation. To confirm whether or not the glucose-alanine cycle has a causal relationship with the observed effect, a secondary