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Hypertriglyceridemia in LR11‐deficiency mice
Author(s) -
Zhu Yanjuan,
Hui David Y
Publication year - 2006
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.20.4.a84-c
Subject(s) - medicine , endocrinology , triglyceride , ldl receptor , postprandial , biology , lipoprotein , cholesterol , chemistry , diabetes mellitus
A relative new comer to LDL receptor family is a protein with 11 LDL receptor ligand binding repeats called LR11. This study has produced LR11‐knockout mice to address the role of this novel receptor in lipid metabolism in vivo. The breeding of LR11 +/− males and females yielded the expected ratio for 1:2:1 for wild type, heterozygous, and homozygous genotype. The animals appeared to thrive normally and didn’t display any gross abnormalities by inspection. LR11+/+ and LR11 −/ − littermates in C57/BL/6 background were maintained on chow diet. Analysis of the plasma lipid levels revealed minimal difference in plasma cholesterol levels between LR11+/+ and LR11−/ − mice under both fasting and fed conditions. Interestingly, the LR11−/ − mice displayed higher plasma triglyceride levels than the LR+/+ mice under both fasting and fed conditions. Analysis of lipoprotein profile by fast performance liquid chromatography of fasting plasma revealed elevated levels of triglyceride‐rich lipoproteins (VLDL fractions 5–8) in LR11−/ − mice compared to that observed in LR11+/+ mice. In fat tolerance test, results showed that plasma triglyceride increased transiently in the wild type mice, with a rapid decline back to basal level within 2 hr. In contrast, the LR11−/ − mice were hypertriglyceridemic after a single fat meal with sustained elevation of plasma triglyceride level for over 2+ hours. Plasma triglyceride levels at 4 hr after lipid meal feeding remained elevated in LR11−/ − mice compared to that observed in the wild type LR11+/+ controls. Taken together, these results suggest that delay postprandial lipid clearance is at least one pathophysiologic condition of LR11 deficiency.