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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Apolipoprotein A5 and hypertriglyceridemia in Prague hypertriglyceridemic rats
M Kadlecová1, S Hojná, R Bohuslavová
1Institute of Physiology AS CR and Cardiovascular Research Center, Prague, Czech Republic.
Physiological Research
|October 22, 2005
Summary
Apolipoprotein A5 (Apoa5) gene variations do not cause hypertriglyceridemia in Prague hereditary hypertriglyceridemic rats. Apoa5 gene expression levels also do not explain the condition or fructose-induced triglyceride increases.
Area of Science:
- Genetics
- Metabolic Syndrome
- Cardiovascular Disease Risk Factors
Background:
- High plasma triglyceride (TG) levels are a significant risk factor for coronary heart disease.
- The Apolipoprotein A5 (Apoa5) gene influences plasma TG concentrations in humans and mice.
- Prague hereditary hypertriglyceridemic (HTG) rats serve as a model for human hypertriglyceridemia and metabolic syndrome.
Purpose of the Study:
- To investigate the role of the Apoa5 gene variation and expression in HTG rats.
- To compare Apoa5 in HTG rats with normotriglyceridemic Lewis and Wistar rat controls.
- To assess Apoa5's response to chronic fructose loading in HTG rats.
Main Methods:
- Screening of Apoa5 gene coding regions and intron-exon boundaries in HTG rats and controls.
- Quantification of Apoa5 gene expression under basal conditions and after fructose loading.
- Measurement of plasma TG levels in HTG rats and controls.
Main Results:
- No mutations in the Apoa5 gene were found in HTG rats compared to controls.
- Basal Apoa5 expression was lower in HTG rats across all age groups.
- Chronic fructose loading significantly increased plasma TG in HTG rats but did not alter Apoa5 expression.
Conclusions:
- Apoa5 gene variation is not the genetic determinant of hypertriglyceridemia in HTG rats.
- The lack of Apoa5 expression changes during fructose-induced TG elevation suggests it does not play a major compensatory role.

