High-Fructose Diet-Induced Hypertriglyceridemia Is Associated With Enhanced Hepatic Expression of ACAT2 in Rats
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
31647302
DOI
10.33549/physiolres.934226
PII: 934226
Knihovny.cz E-resources
- MeSH
- Sterol O-Acyltransferase biosynthesis genetics MeSH
- Gene Expression MeSH
- Fructose administration & dosage adverse effects MeSH
- Hypertriglyceridemia chemically induced genetics metabolism MeSH
- Liver drug effects metabolism MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Sterol O-Acyltransferase 2 MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Sterol O-Acyltransferase MeSH
- Fructose MeSH
High levels of fructose induce hypertriglyceridemia, characterized by excessive levels of triglyceride-rich lipoproteins such as very low-density lipoprotein (VLDL); however, the underlying mechanisms are poorly understood. The aim of this short communication was to examine hepatic changes in the expression of genes related to cholesterol metabolism in rats with hypertriglyceridemia induced by high-fructose or high-glucose diets. Rats were fed a 65 % (w/w) glucose diet or a 65 % (w/w) fructose diet for 12 days. Serum levels of triglycerides, total cholesterol, and VLDL+LDL-cholesterol, hepatic levels of triglycerides and cholesterol, and ACAT2 expression at the gene and protein levels were significantly higher in the fructose diet group compared to the glucose diet group. The hepatic levels of Abcg5/8 were lower in the fructose group than in the glucose group. Serum high-density lipoprotein (HDL)-cholesterol and hepatic expression levels of Hmgcr, Ldlr, Acat1, Mttp, Apob, and Cyp7a1 did not differ significantly between groups. These findings suggest that high-fructose diet-induced hypertriglyceridemia is associated with increased hepatic ACAT2 expression.
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