EFFECTS OF INSULIN-TREATMENT OF DIABETIC RATS ON HEPATIC PARTITIONINGOF FATTY-ACIDS BETWEEN OXIDATION AND ESTERIFICATION, PHOSPHOLIPID ANDACYLGLYCEROL SYNTHESIS, AND ON THE FRACTIONAL RATE OF SECRETION OF TRIACYLGLYCEROL IN-VIVO

1. The hypothesis that insulin treatment of streptozotocin-diabetic ra ts does not alter acutely the ability of acylcarnitine synthesis to co mpete successfully for cytosolic long-chain acyl-CoA [Grantham and Zam mit (1988) Biochem. J. 249, 409-414], was tested in vivo by using the technique of selective labelling of hepatic fatty acids in awake unres trained rats. In the same animals, the partitioning of hepatic fatty a cids between acylglycerol and phospholipid synthesis, and of newly lab elled triacylglycerol between secretion into the plasma and retention in the liver, was also studied. 2. In untreated diabetic animals, the ratio of fatty acid oxidation to esterification was double that found in normal fed animals, whereas there were no differences in the values of the above-mentioned parameters of glycerolipid metabolism. Thus th e insulin status of the rats only has chronic effects on specific aspe cts of fatty acid metabolism in the liver. 3. Treatment of diabetic ra ts with insulin resulted in no change in the oxidation/esterification ratio for the first 5 h after the start of insulin administration. The reafter, there were reciprocal changes in the (CO2)-C-14 expired (an i ndex of oxidation) and C-14 label recovered in hepatic and plasma glyc erolipids. However, the pattern of partitioning observed in normal fed rats was still not re-established after 8 h of insulin treatment. 4. There was a small and transient decrease in the fractional rate of tri acylglycerol secretion by the liver at the start of insulin treatment and an increase in the proportion of labelled fatty acid that was util ized for phospholipid synthesis such that phospholipid labelling as a proportion of that of total glycerolipids was doubled after 8 h of ins ulin treatment. 5. The data are discussed in relation to the roles of insulin in mediating acute changes in hepatic fatty acid metabolism an d very-low-density-lipoprotein triacylglycerol secretion by the liver.