Preferential retention of linoleic acid-enriched triacylglycerols in liver and serum during fasting.

Fasting has been reported to quantitatively increase linoleic and arachidonic acids in liver triacylglycerols, but the origin and mechanism of this change are unknown. The changes in long-chain fatty acids and triacylglycerol species of liver, serum, adipose tissue, and heart were therefore examined during a period of 24- or 48-h fasting in the rat. In liver and serum triacylglycerols, fasting resulted in a quantitative increase in arachidonic, stearic, linoleic, alpha-linolenic, and docosahexaenoic acids but a decrease in oleic, palmitic, and palmitoleic acids. After fasting, oleic acid was depleted the most from liver and serum triacylglycerols followed by palmitoleic and palmitic acids. Triacylglycerol species containing palmitic, palmitoleic, and oleic acids were depleted the most from liver and serum during fasting. Linoleic acid-enriched triacylglycerol species were proportionally and, in some cases, quantitatively increased in liver and serum triacylglycerols during fasting. Net retention of triacylglycerol species with a total acyl carbon number of 56 or 58 in the liver and 60 in serum was also observed during fasting. Selective retention of triacylglycerol species did not occur in the heart or perirenal or epididymal adipose tissue during fasting. Tissue phospholipid fatty acids were largely unaffected by fasting. Our data suggest that during fasting, long-chain fatty acids released from adipose tissue are differentially utilized and hepatic triacylglycerol species are remodeled, permitting optimal tissue composition of essential fatty acids, particularly linoleic acid.