The effect of myo-inositol deficiency on lipid metabolism in rats : II. The mechanism of triacylglycerol accumulation in the liver of myo-inositol-deficient rats

Abstract

1. 1. The mechanism of the triacylglycerol accumulation in liver which had been observed in the myo-inositol-deficient rats (the preceding paper, Hayashi E., Maeda T. and Tomita T. (1974) Biochim. Biophys. Acta 360, 134–145) has been investigated. 2. 2. Fatty acid distribution in the deposited triacylglycerols was quite similar to that of epididymal fat pads and to that of the dietary fat. 3. 3. Reserpine treatment caused a reduction in serum non-esterified fatty acids and dramatically reduced the accumulation of triacylglycerols and cholesterol in the liver. 4. 4. Incorporation of [1- 14C]palmitate from the specifically labelled epididymal fat pads to liver lipids in the deficient rats was 2.7 times that of the control rats. 5. 5. Disappearance of intravenously injected [1- 14C]palmitate from liver was somewhat accelarated in the deficient rats. 6. 6. Incorporation of [1- 14C] acetate into liver fatty acids and that of [1- 14C] palmitate into liver triacylglycerols was unaltered. 7. 7. The l-glycerol 3-phosphate level in the liver was decreased by 25% and 38% after one and two weeks, respectively, of myo-inositol-deficiency treatment. 8. 8. The above results indicate that an accumulation of triacylglycerols in the liver of the myo-inositol-deficient rats is primarily due to an increased rate of fatty acid mobilization from adipose depots to the liver.