Changes in fatty acid oxidation of peroxisomes in the liver of alloxan-diabetic rats were studied. After injection of alloxan (150 mg/kg, subcutaneously), the activity of peroxisomal cyanide-insensitive beta-oxidation increased more rapidly than that of carnitine palmitoyltransferase, which was the rate-limiting step of mitochondrial beta-oxidation, and reached 3 times the control level at 7 days after the treatment. The peroxisomal beta-oxidation activity was more potent toward medium chain acyl-CoAs (C=10 and 12), though it was extremely low for shorter chain lengths. The activity of carnitine acetyltransferase increased to 2.4 times the control level and the change appeared mainly in the peroxisomal fraction. On the other hand, the activity of palmitoyltransferase increased to twice the control level, distributed mostly in the mitochondrial fraction. The activity of carnitine acyltransferase increased mainly in the peroxisomal fraction, and was higher for shorter and medium chain acyl-CoAs. These results suggest that peroxisomal fatty acid oxidation and transport of acetyl-CoA and medium chain acyl-CoA as well as NADH product in peroxisomes may be rapidly enhanced in response to the demand of organs for the urgent supply of energy from fatty acids in the diabetic condition.

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In the livers of fasted rats, the activity of peroxisomal palmitocyl-CoA oxidation (NADH production) was increased more rapidly and markedly than that of mitochondrial carnitine palmitoyltransferase, which is the rate limiting enzyme of mitochondrial beta-oxidation. The peroxisomal oxidizing activity was about twice that of the control throughout the period of fasting (1-7 days). carnitine acetyltransferase activity was increased to a similar extent in both peroxisomes and mitochondria. A possible physiological role of liver peroxisomes may thus be as an effective supply of NADH2, acetyl residues and short and medium-length fatty acyl-CoA in the cells on the enhancement of peroxisomal beta-oxidation of the animals under starvation; these substances thus produced may be transported into the mitochondria as energy sources.

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