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Titolo:
Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E
Autore:
Hirano, T; Takahashi, T; Saito, S; Tajima, H; Ebara, T; Adachi, M;
Indirizzi:
Showa Univ, Sch Med, Dept Internal Med 1, Shinagawa Ku, Tokyo 1428666, Japan Showa Univ Tokyo Japan 1428666 Med 1, Shinagawa Ku, Tokyo 1428666, Japan
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
fascicolo: 4, volume: 281, anno: 2001,
pagine: E665 - E669
SICI:
0193-1849(200110)281:4<E665:ACDMST>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEPARAN-SULFATE PROTEOGLYCANS; APOLIPOPROTEIN-E; TRANSGENIC MICE; LIPOPROTEIN METABOLISM; RICH LIPOPROTEINS; APO-CIII; HYPERTRIGLYCERIDEMIA; RATS; OVEREXPRESSION; ACCUMULATION;
Keywords:
apoprotein C-III; apoprotein E; triglyceride secretion; mice;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Hirano, T Showa Univ, Sch Med, Dept Internal Med 1, Shinagawa Ku, 1-5-8 Hatanodai, Tokyo 1428666, Japan Showa Univ 1-5-8 Hatanodai Tokyo Japan 1428666 o 1428666, Japan
Citazione:
T. Hirano et al., "Apoprotein C-III deficiency markedly stimulates triglyceride secretion in vivo: comparison with apoprotein E", AM J P-ENDO, 281(4), 2001, pp. E665-E669

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 investigatethe 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 anextent 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 TGproduction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 16:05:06