Phosphorus metabolism in unsaturated fatty acid-deficient rats.

The gross symptoms of essential fatty acid deficiency have been known for more than 20 years (l-3), but the origin of the increased metabolic rate, increased water consumption, and eventual growth failure which characterize the syndrome have not been traced to a particular area of intermediary metabolism. An involvement of oxidative processes with unsaturated fatty acid deficiency has been shown by Kunkel and Williams (4) who reported an increased cytochrome oxidase activity in livers from fat-deficient rats. An attempt has been made in the present study to investigate further the aspects of metabolism which are dependent upon the unsaturated fatty acids for their proper function. Measurements of radioactive phosphorus (P”“) uptake suggested that in a fat deficiency there was an altered phosphorus (P) metabolism associated with either glycolytic or respiratory mechanisms. Studies carried out in vitro showed that the deficiency results in a decreased esterification of high energy phosphate during the oxidation of some of the tricarboxylic acid cycle intermediates. This decreased esterification has been localized at or about the level of electron transport concerned with diphosphopyridine nucleotide (DPN).