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The role of MCPIP‐1 in maintaining lipid homeostasis (LB156)
Author(s) -
Moody Joshua,
Sedinkin Jessica,
Chang Yingzi
Publication year - 2014
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.28.1_supplement.lb156
Subject(s) - triglyceride , very low density lipoprotein , cholesterol , medicine , endocrinology , homeostasis , lipid metabolism , lipoprotein , chemistry , lipid profile , blood lipids , inflammation , biology
Background:Increased inflammation is associated with alterations of lipid and lipoprotein metabolism. Recent studies suggest that MCPIP1 (Monocyte Chemotactic Protein induced Protein‐1) may have a role in maintaining normal metabolic balance by negatively regulating chronic inflammation. Our preliminary data revealed that the MCPIP1 deficient (MCPIP1‐/‐) mice have reduced body lipid deposits compared to control mice. The current project was designed to test if MCPIP1 is involved in maintaining lipid homeostasis by affecting hepatic lipid production and distribution. Methods: MCPIP1‐/‐ mice (C57/BL6 background, 6 weeks old) were identified by PCR. The serum and liver from control and MCPIP1‐/‐ mice were collected after fasting. Serum lipids (LDL/VLDL‐cholesterol and total triglyceride) and liver lipids (total cholesterol and triglyceride) were measured using commercially available kits. Results: The data collected from sixteen samples (eight control and eight MCPIP1‐/‐) showed that in MCPIP1 ‐/‐ mice the mean serum HDL‐cholesterol and total triglyceride concentrations were about 49% and 31% lower respectively, compared to control mice. In contrast, serum concentration of LDL/VLDL‐cholesterol in MCPIP1‐/‐ mice increased about 66% when compared to control. Triglyceride in the liver tissue of MCPIP‐/‐ mice was also drastically decreased (72% lower than control). No changes were observed in total cholesterol in liver tissue. Conclusion: The lack of MCPIP1 is associated with alterations of lipid homeostasis. Grant Funding Source : Supported by KCOM Graduate Program in Biomedical Sciences