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We studied the relationships among levels of acid cholesteryl esterase (ACE) activity in kidney, liver, and aorta and clearance of125I-labeled human low density lipoprotein (LDL) from the circulation. The premise was that levels of ACE (which is involved in the hydrolysis of the cholesteryl esters of LDL) might correspond to the rate at which LDL was removed from the circulation, or fractional catabolic rate (FCR). The models used were rats with streptozotocin diabetes and^ exercised (swimming) rats. In the diabetic rat, ACE specific activity was increased by 46% in kidney and 30% in liver and decreased by 25% in aorta when compared to controls. The FCR of LDL increased by 25% in the diabetic animal over control values. Insulin treatment restored all these alterations to normal. Swimming rats showed no change in ACE-specific activity of kidney or liver, but aortic ACE increased by approximately 25% over levels in sedentary rats. The FCR of radioiodinated LDL in swimmers was unchanged from normal. Return of swimmers to a sedentary existence resulted in persistence of normal ACE activity in kidney and liver and in FCR of LDL; however, previously elevated aortic ACE activity returned to normal. Thus, dynamic, irreversible removal of LDL from the circulation (FCR) is changed in the same direction as, and may be linked to, ACE activity in non-vascular tissues. Aortic ACE activity, on the other hand, is not so related to either ACE in those tissues or to FCR of LDL. One implication of this finding is that the general pattern of LDL catabolism by the rat is distinct from the local problem of LDL catabolism by the blood vessel wall. Circ Res 47: 433-442, 1980

circulation research

Hydrolase activities in the rat aorta. IV. Relation between clearance rates of circulating 125I-labeled low-density lipoproteins and levels of tissue hydrolase activity.