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Some Biochemical Lesions Associated with Liver Fat Accumulation in Threonine-deficient Rats1

Dorothy Arata, Catherine Carroll2 and Dena C. Cederquist

Department of Foods and Nutrition, College of Home Economics, Michigan State University, East Lansing, Michigan

The metabolism of 2 groups of co-factors, the pyridine nucleotides and the adenosine polyphosphates, was altered in fatty livers produced in weanling rats by feeding a low protein diet deficient in threonine. Both total pyridine nucleotide levels and the PN/PNH ratio were significantly decreased by the twenty-fifth day in livers from threonine-deficient animals. These values returned to control levels upon subsequent supplementation with threonine. The amount of labile phosphorus derived from ADP and ATP from the fatty livers was significantly less than that from livers of control rats. The activity of the DPN-cytochrome c reductase enzyme system was significantly lower in livers from threonine-deficient rats than in livers from threonine-supplemented rats throughout the experimental period. The activity of the fatty acid oxidase system declined sharply during the early stages of fat accumulation in the liver. The subsequent, complete recovery of this enzyme system was followed closely by a return of liver fat concentrations to near-control levels. The ultimate dependence of all the above functions on active electron transport is noted, and the suggestion made that a threonine deficiency might affect some phase of this system.


1 Supported in part by United States Air Force contract no. AF 49(657-276). Journal Article no. 3201 from the Michigan Agricultural Experiment Station.

2 Present address: Department of Home Economics, University of Arkanasas, Fayetteville, Arkansas.

Manuscript received 5 August 1963.





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