The effects of streptozotocin diabetes on hepatic triglyceride lipase activity in the rat

Abstract

The function of the hepatic triglyceride lipase (H-TGL) is not yet clear. The purpose of the present study was to investigate the possible hormonal regulation of H-TGL. Postheparin plasma was obtained 3 min after the intravenous injection of 50 U/250 g body weight of heparin into male Wistar rats. The lipase activities were measured using substrate containing [ 14C] triolein emulsified with gum arabic and were expressed in μmoles of free fatty acid released/ml/hour (mean ± SD). H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl. Diabetic rats were prepared by intravenous injection of streptozotocin (STZ), 65 mg/kg body weight. The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection. H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations. H-TGL was significantly higher at 3 min after the injection of 50 U of heparin/250 g body weight than at 20 min. Twenty-four-hour fasting produced a significant fall in H-TGL compared to H-TGL in fed rats. Total TGH was significantly lower in diabetic rats 3 days after STZ injection. In diabetic rats 3, 5, and 7 days after STZ injection, H-TGL were significantly lower than those in control rats. H-TGL and H-TGL/total TGH were 9.49 ± 0.99 and 0.551 ± 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 ± 0.69) and H-TGL/total TGH (0.739 ± 0.052) in control nondiabetic rats. When diabetic rats were treated with insulin, total TGH (14.37 ± 3.01) and H-TGL (6.77 ± 4.12) rose to 25.16 ± 1.02 (total TGH) and 16.46 ± 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats. Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma. The enzyme activity of peak I from STZ rats, which is eluted by 0.72 M NaCl-Veronal buffer, pH 7.4 and corresponds to H-TGL, was approximately half the activity from control rats. TGH released by heparin from isolated rat liver parenchymal cells was investigated. The enzyme activities released from isolated liver parenchymal cells prepared from STZ rats was approximately half that from control rats. The role of insulin in the regulation of LPL has been well documented. Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.