Abstract

Weber-Christian disease with hypertriglyceridemia (Type IV) was 29 years old male. Apolipoprotein C-II content in his whole serum was normal. Post heparin lipolytic activity was decreased with an increase in plasma volume as an enzyme solution. These results suggested that inhibitory factor existed in this patient plasma. Purified human and bovine milk lipoprotein lipase (LPL) activities were also inhibited by the addition of his plasma.VLDL-hydrolysis by milk LPL was inhibited by the addition of his plasma. The inhibitory factor in this patient did not inhibit carboxylesterase activity suggesting no inhibition of catalytic site of lipasea) and did not inhibit the VLDL-LPL complex formation suggesting no inhibition of substrate recognition site. But the factor inhibited the dipalmitoyl phosphatidylcholine-activated carboxylesterase activity. These results suggest that the factor inhibits the catalytic site revealing process of LPLa).(a: Shirai K. and Jackson R. L. J. Biol. Chem. 257, 1253, 1982)

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