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Am J Physiol Endocrinol Metab 281: E665-E669, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 4, E665-E669, October 2001

Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E

Tsutomu Hirano, Toshihiro Takahashi, Shigenobu Saito, Hiroto Tajima, Tetsu Ebara, and Mitsuru Adachi

First Department of Internal Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan

Apoprotein (apo) C-III plays an important role in the development of hypertriglyceridemia by inhibiting triglyceride (TG) removal. However, the effect of apo C-III on TG production remains unclear. We measured TG secretion rate (TGSR) in apo C-III gene-disrupted (apo C-III-null) mice to investigate the influence of this protein on TG turnover. TGSR measured by the Triton WR-1339 method was increased twofold in these mice compared with wild-type (WT) mice. Obesity was induced by the injection of gold-thioglucose (GTG), which made the WT mice hypertriglyceridemic due to a threefold increase of TGSR. However, GTG-induced obesity failed to increase TG in apo C-III-null mice, although TGSR was increased 10-fold, suggesting substantial stimulation of TG removal. Apo E-null mice were severely hypercholesterolemic but were not hypertriglyceridemic, and TGSR was rather decreased. GTG-induced obesity made these mice hypertriglyceridemic because of TG overproduction to an extent similar to that seen in WT mice. These results suggest that apo C-III deficiency potently enhances TG turnover, especially when TG production is stimulated, and that apo E deficiency is not always rate limiting for TG production.

apoprotein C-III; apoprotein E; triglyceride secretion; mice


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