Hepatic High Energy Phosphate Metabolism in Transgenic Livers Expressing Creatine Kinase as Revealed by 31P NMR

There is no consensus for a detailed model of the regulation of mitochondrial ATP production in cells. The problem of metabolic control in intact tissues is extremely difficult for two reasons. First, it is not clear how best to measure the parameters believed to be important in control of mitochondrial metabolism. Second, it is difficult to make specific perturbations in order to test possible models of metabolic control. The ability to alter an animaľs genome using transgenic techniques in combination with nondestructive spectroscopic tools, such as NMF., offers solutions to these two problems. In this paper, we describe recent work that has made use of a transgenic mouse model that expresses the enzyme, creatine kinase in liver. Creatine kinase is not normally expressed to any appreciable extent in liver. 31 P NMR studies of these transgenic livers have supplied information about the regulation of ATP catabolism, the role of creatine kinase in ATP metabolism, and the quantitative control of oxidative phosphorylation by ADP.