Abstract
We have previously suggested that mechanisms other than reduced lipoprotein lipase (LPL) activity might contribute to the defect in plasma removal of very low density lipoprotein (VLDL)-triglyceride (TG) observed in insulin-deficient rats. To further evaluate this phenomenon, removal rates of TG in nonfractionated plasma, as well as in isolated lipoprotein fractions obtained from insulin-deficient and control rats, were compared in a new, sensitive in vivo bioassay system (estradiol-treated male rats with a consistently low endogenous VLDL-TG pool). Removal of TG in nonfractionated plasma from insulin-deficient rats was slower than that of control rats: 3.0 +/- 0.3 vs 1.6 +/- 0.2 min (P less than 0.001). No difference was found in removal rate of isolated VLDL-TG (2.5 +/- 0.3 vs 2.6 +/- 0.4 min), or in removal rates of TG carried in other lipoprotein fractions. We next determined the effect of injection into normal rats of aliquots of dialyzed lipoprotein-free (D greater than 1.215) plasma from insulin-deficient and control rats on the removal rate of normal VLDL-TG, and found that lipoprotein-free plasma from insulin-deficient rats significantly (P less than 0.01) prolonged removal of normal VLDL-TG (4.3 +/- 0.4 to 6.8 +/- 0.7 min). This same fraction did not interfere with the in vitro hydrolysis of normal VLDL-TG by post-heparin LPL. Thus, a factor in the D greater than 1.215 plasma fraction of insulin-deficient rats is present which interferes with the rate of removal of TG from plasma, unrelated to inhibition of LPL activity.
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