Apolipoprotein A5 and hypertriglyceridemia in Prague hypertriglyceridemic rats
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
16238453
DOI
10.33549/physiolres.930876
PII: 876
Knihovny.cz E-zdroje
- MeSH
- apolipoprotein A-V MeSH
- apolipoproteiny genetika MeSH
- fruktosa farmakokinetika MeSH
- hypertriglyceridemie genetika metabolismus MeSH
- introny MeSH
- krysa rodu Rattus MeSH
- metabolický syndrom krev genetika MeSH
- molekulární sekvence - údaje MeSH
- mutantní kmeny potkanů MeSH
- potkani inbrední LEW MeSH
- potkani Wistar MeSH
- sekvence nukleotidů MeSH
- tělesná hmotnost MeSH
- triglyceridy krev MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- Apoa5 protein, rat MeSH Prohlížeč
- apolipoprotein A-V MeSH
- apolipoproteiny MeSH
- fruktosa MeSH
- triglyceridy MeSH
High plasma triglyceride (TG) level is a major independent risk factor of coronary heart disease. A newly identified Apolipoprotein A5 (Apoa5) gene has been shown to play an important role in determining plasma TG concentrations in humans and mice. Prague hereditary hypertriglyceridemic (HTG) rats are a useful model of human hypertriglyceridemia and other symptoms of metabolic syndrome. Thus, the variation of Apoa5 gene and its expression were studied in this strain under normal conditions and after chronic fructose loading. Lewis and Wistar rats served as normotriglyceridemic controls. Plasma TG were significantly higher in HTG rats in comparison with both control strains. Screening of the coding regions and intron-exon boundaries of Apoa5 gene did not reveal any mutation of this gene in HTG rats in comparison with Lewis and Wistar ones. However, rat Apoa5 gene contains only one intron in contrast with two introns of mouse Apoa5 gene. Under the basal conditions the expression of Apoa5 was lower in all age groups of HTG rats compared to Wistar animals. Furthermore, during chronic fructose loading there were no significant changes of Apoa5 expression in HTG rats, although plasma TG levels rose 3-4 times within first two days of fructose loading and were increased during the whole period of fructose treatment. In conclusion, Apoa5 does not seem to be a genetic determinant of hypertriglyceridemia in HTG rats. The absence of significant changes in Apoa5 gene expression during chronic fructose-induced TG elevation excludes its major role in mechanisms compensating severe hypertriglyceridemia.
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