Energy metabolism gluconeogenesis

Modulates energy metabolism, Gluconeogenesis—interactions. With FOXOl and FOXA2... 

During periods of hunger, muscle proteins serve as an energy reserve for the body. They are broken down into amino acids, which are transported to the liver. In the liver, the carbon skeletons of the amino acids are converted into intermediates in the tricarboxylic acid cycle or into acetoacetyl-CoA (see p. 175). These amphibolic metabolites are then available to the energy metabolism and for gluconeogenesis. After prolonged starvation, the brain switches to using ketone bodies in order to save muscle protein (see p. 356). 

T. Kashiwagura, C.J. Deutsch, J. Taylor, M. Erecinska, D.F. Wilson, Dependence of gluconeogenesis, urea synthesis, and energy metabolism of hepatocytes on intracellular pH, J. Biol. Chem. 259 (1984) 237-243. 

The gluconeogenesis pathway shown as part of the essential pathways of energy metabolism. The numbered reactions are unique to gluconeogenesis. (See Figure 8.2, p. 90 for a more detailed view of the metabolic map.)... 

Aconitase (ACO) is a mitochondrial protein that acts as the second enzyme in the TCA cycle contributing to overall energy production. Aconitase activity is significantly reduced in the striatum and cortex of HD individuals thereby yielding in overall decrease of ATP production (Sorolla et al. 2008). Mitochondrial dysfunction, which is observed in HD, can occur via the oxidative modification of aconitase (Petrozzi et al. 2007). Decreased ATP production due to lipid peroxidation can lead to altered energy metabolism and reduced gluconeogenesis, which have been associated with HD pathogenesis (Josefsen et al. 2010). 

Proteins are hydrolysed in the stomach by pepsin to form amino acids. Further hydrolysis occurs in the intestine. The amino acids are absorbed. Any amino acids in excess of those needed to replace the wear and tear of tissues, and for biosynthesis to hormones, pyrimidines, purines, etc., are used for gluconeogenesis, or for energy metabolism. However, catabolism of amino acids generates ammonium ions (NH4+), which are very toxic. Accordingly, NH/ is disposed of by conversion to urea which is non-toxic and is readily excreted via the kidney. 

Garber, A. J., Ballard, F. J., and Hanson, R. W., 1972, Significance of mitochondrial phosphoenolpyruvate formation in the regulation of gluconeogenesis in guinea pig liver, in Energy Metabolism and the Regulation of Metabolic Processes (R. W. Hanson and M. A. Mehlman, eds.), p. 109, Academic Press, New York. 

---