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The effect of fatty acids on the synthesis of P‐enolpyruvate by human liver mitochondria
Author(s) -
Jomain-Baum Mireille,
Hanson Richard W.
Publication year - 1973
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(73)80546-0
Subject(s) - medical school , library science , citation , human services , medicine , gerontology , political science , law , medical education , computer science
Most of the studies of the regulation of gluconeogenesis in mammalian liver have been carried out using the rat and have pointed to a key role for the enzyme P-enolpyruvate carboxykinase (E C 4. 1. 1. 2) [l-3]. In this species the hepatic enzyme is almost totally cytosolic and is induced by a variety of dietary and hormonal affecters [4-71. More recently, work with other species such as the guinea pig [2,8,9], rabbit [lo] and cat [ 1 l] , all of which contain SO-60% of their total P-enolpyruvate in the mitochondria, has indicated that the regulation of hepatic gluconeogenesis in these animals may be different from that in rat liver. The mitochondrial formation of P-enolpyruvate is of considerable importance in gluconeogenesis in guinea pig and rabbit liver [ 121 and is markedly decreased by both fatty acids and fi-hydroxybutyrate which act by increasing mitochondrial NADH levels [9, IO]. These compounds also inhibit gluconeogenesis from lactate and alanine in the isolated, perfused liver from both species and stimulates it in rat liver [8, 13151. The difference in the regulation of glucose synthesis in guinea pig and rabbit liver as compared to rat liver underlines the difficulties in generalizing about the control of important metabolic processes between species. This is of critical importance since human liver