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Caveolin‐3 KO Mice Develop Dyslipidemia with Impaired Substrate Utilization in Skeletal Muscle.
Author(s) -
Capozza Franco,
Trimmer Casey,
Lisanti Michael P
Publication year - 2009
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.23.1_supplement.600.32
Subject(s) - skeletal muscle , dyslipidemia , sarcolemma , caveolae , caveolin 3 , endocrinology , medicine , insulin resistance , myocyte , caveolin , caveolin 1 , chemistry , biology , microbiology and biotechnology , diabetes mellitus , signal transduction
Caveolin‐3 (Cav‐3) is expressed predominantly in skeletal muscle fibers where it drives Caveolae formation at the muscle cell's plasma membrane (sarcolemma). We and others have previously shown that mice with a genetic ablation of Cav‐3 develop glucose intolerance, insulin resistance, and obesity. The main objective of this study is to determine the effect of Cav‐3 ablation on whole‐body/tissue lipid metabolism. To address this issue, several metabolic parameters were analyzed in the plasma of young and older Cav‐3 KO mice. In addition, by employing radiolabeled metabolic substrates, we directly determined the contribution of skeletal muscle to the plasma dyslipidemia of Cav‐3 KO mice. In summary, the current study shows that an absence of Cav‐3 leads to dyslipidemia in mice. The primary defect can be localized to the skeletal muscle and is secondary to altered muscle substrate utilization caused by Cav‐3 ablation. Support: American Heart Association; BGIA