The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E
Abstract
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.
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In the citing paper
“To determine how the mutation affected overall synthesis and secretion of triglycerides, we injected the mice with Triton WR-1339, which inhibits lipolysis and lipoprotein clearance (27), and measured plasma triglycerides at various time points (Supplemental Figure 1).”
From Syndecan-1 is the primary heparan sulfate proteoglycan mediating hepatic clearance of triglyceride-rich lipoproteins in mice (2009) · cites this paper as [27]
In the citing paper
“MB47 does not bind to murine apoB-100.”
From Liver heparan sulfate proteoglycans mediate clearance of triglyceride-rich lipoproteins independently of LDL receptor family members (2007) · cites this paper as [52]
Citations
Cites
Hypertriglyceridemia as a Result of Human apo CII Gene Expression in Transgenic Mice
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“A number of clinical and experimental studies have demonstrated that apo C-III inhibits the action of lipoprotein lipase, a key enzyme in TG hydrolysis (6, 9, 14), and inhibits the hepatic uptake of TG-rich lipoprotein (TGRL) particles (14, 23).”
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Cited by
Sorted by citations
Pathophysiology of Diabetic Dyslipidemia
Hirano, T. (2018) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv17023 · Cited by 552
Self-citationStanford, K. I., Bishop, J. R., Foley, E. M., Gonzales, J. C., Niesman, I. R., Witztum, J. L., & Esko, J. D. (2009) · Journal of Clinical Investigation · doi:10.1172/jci38251 · Cited by 226
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Willems van Dijk, K., Rensen, P. C., Voshol, P. J., & Havekes, L. M. (2004) · Current Opinion in Lipidology · doi:10.1097/00041433-200406000-00002 · Cited by 154
Metadata
- Authors
- Hirano, T., Takahashi, T., Saito, S., Tajima, H., Ebara, T., & Adachi, M.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2001-10-01
- Volume
- 281
- Issue
- 4
- Pages
- E665-E669
- ISSN
- 0193-1849
- 1522-1555
- Cited by
- 19
- References
- 2
- Language
- en
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