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Functions of Monocyte Chemotactic Protein‐3 in Transgenic Mice Fed High‐fat Diet
Author(s) -
An So Jung,
Choi Myung-sook,
Chae Chan Kyu,
Oh Goo Taek,
Park Yong Bok
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.991.4
Subject(s) - endocrinology , medicine , genetically modified mouse , cholesterol , transgene , monocyte , biology , triglyceride , chemistry , biochemistry , gene
In order to look into the function of the monocyte chemotactic protein‐3 (MCP‐3) in the atherogenesis, transgenic mice in which the MCP‐3 is over‐expressed in a specific tissue (vesicular endothelium) have been produced in the previous work, genotyped by a specific primer set designed from the MCP‐3 cDNA and fed high‐fat‐high‐cholesterol diet for 12 weeks to provide extreme atherogenic conditions. In the level of plasma lipids, the mice fed HFHC diet showed a higher level of total cholesterol and lower in the triglyceride level. On the other hand, the level of HDL‐cholesterol was surprisingly increased in the mice fed normal diet showing 72.6 in the HTR (HDL vs. total cholesterol ratio). Accordingly, the atherogenic index of the mice fed a normal diet was drastically lower than in the wild‐type mice. This was supported through a marked increase in the expression of Apo‐AI gene in the transgenic mice fed normal diet identified by microarray analysis. Activities of anti‐oxidant enzymes were also increased in the transgenic mice fed HFHC diet, indicating that there might be more oxidative damage to tissues of the mice fed HFHC diet leading to a progress toward the atherosclerosis. Supplementation of anti‐oxidants to the diet, naringin and hesperidin, was shown to lower the level of the activities of anti‐oxidant enzymes.