Abstract
Allylisopropylacetamide (AIA), when administered to rats, induces high levels of hepatic mitochondrial δ-aminolevulinic acid synthetase (ALA synthetase). The activity of this enzyme can be quantitated in porphyric rat liver, since the freshly prepared mitochondria from porphyric rat liver are permeable to succinyl-coenzyme A and do not have high deacylase activity. Administration of carbohydrate to rats markedly inhibits the induction of ALA synthetase by AIA. Since ALA synthetase is thought to be the rate controlling enzyme in hepatic porphyrin biosynthesis, diet is a regulatory factor in hepatic porphyrin synthesis in porphyria. The previously observed effects of diet on porphyrin precursor excretion in both experimental and human acute intermittent porphyria are best explained by the effect of diet on the hepatic ALA synthetase level. The application of the theory of “catabolite repression” to the present findings is discussed.
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