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Concomitant Repression by Gluten of HMP Shunt Dehydrogenases, Citrate Cleavage Enzyme and Malic Enzyme in Rat Liver and Adipose Tissue1

Gaetano Livrea, Giovanni Carrozza, Luigi Manasseri and Ugo Muraca

Istituto di Fisiologia Umana dell'Università di Messina, 98100 Messina, Italy

On the basis of previous results which indicate that a gluten diet represses hexose monophosphate shunt dehydrogenases (HMPD) in the rat liver, the activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), citrate cleavage enzyme (CCE) and malic enzyme (ME), as well as plasma insulin levels, were examined in the liver and epididymal fat pad of male rats fed diets containing as their nitrogenous component, either casein, gluten, or gluten supplemented with Lys and Thr after protein deprivation. The gluten diet repressed the activities of HMPD, CCE and ME. The intensity and the nature of the repression was different in liver and in adipose tissue. In the liver the repression of HMPD was greater than that of CCE and ME and in no case was the enzyme repression prevented by addition of Lys and Thr to the gluten diet. In the adipose tissue the repression of CCE and ME was greater than that of HMPD and in all cases the repression was prevented by addition of Lys and Thr. The enzyme responses were independent of any direct effect of the diets on insulin secretion and, as might be inferred from the constant levels of liver glycogen, independent of any effect on other hormones involved in the coordination of various phases of lipid metabolism and in its integration with carbohydrate metabolism. These results are consistent with the view that in the liver the levels of lipogenic enzymes are controlled by different regulatory mechanisms than in the adipose tissue.


KEY WORDS: • gluten • liver • adipose tissue • HMP shunt dehydrogenases • citrate cleavage enzyme • malic enzyme

1 This investigation has been supported by a research grant from the Consiglio Nazionale delle Ricerche, Italy.

Manuscript received 15 January 1975.





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