| First Author | Hirano T | Year | 2001 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 281 |
| Issue | 4 | Pages | E665-9 |
| PubMed ID | 11551841 | Mgi Jnum | J:72104 |
| Mgi Id | MGI:2151732 | Doi | 10.1152/ajpendo.2001.281.4.E665 |
| Citation | Hirano T, et al. (2001) Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E. Am J Physiol Endocrinol Metab 281(4):E665-9 |
| abstractText | 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. |
