Evidence for Catabolic Defect of Triglyceride in Experimental Nephrosis

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Lipids content, triglyceride (TG) production and its secretion in the liver were examined to explore the mechanism of hypertriglyceridemia (HTG) in puromycin aminonucleoside-induced nephrotic rats. Plasma TG, total cholesterol, phospholipid and apoprotein B concentrations in nephrotic rats were about 4-5 times higher than those in control rats. The HTG in nephrosis was mainly due to the elevation of TG-rich lipoprotein (TRL)-TG concentration. Despite remarkable increase in plasma and TRL lipids levels, lipid contents in liver were not significantly increased in nephrotic rats. [³H]-glycerol was injected into portal vein and the radioactivity of endogenous labeled TG in liverr was measured to access the ability for hepatic TG production. Neither the radioactivity nor the specific activity of TG was increased in nephrotic liver compared to the liver of control rats. Triton WR 1339, a potent inhibitor of TRL-TG removal, was injected to assume TRL-TG secretion rate. TRL-TG secretion rate was not increased in nephrotic rats. In addition, the TG/protein ratio in nephrotic TRL was two times as high as that of control, which was similar to the ratio of TRL in their post-Triton plasma. These results demonstrate that HTG in nephrosis is not simply due to increased hepatic TRL-TG production, but suggest that the catabolic defect of TRL-TG may be the more predominant abnormality to cause substantial HTG in this syndrome.