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Mice with null mutation of Ceacam1 exhibit metabolic syndrome with cardiac hypertrophy
Author(s) -
Morgan Eric E.,
Ledford Kelly J,
DeAngelis Anthony M,
Buehler Jason,
Patel Payal,
Najjar Sonia M,
Khouri Samer,
Pierre Sandrine V
Publication year - 2008
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.22.1_supplement.1226.29
Subject(s) - medicine , endocrinology , hyperinsulinemia , metabolic syndrome , blood pressure , insulin resistance , left ventricular hypertrophy , insulin , cardiology , obesity
Metabolic syndrome is a risk factor for cardiovascular disease. Because the carcinoembryonic antigen‐related cell adhesion molecule 1 ( Ceacam1 ) regulates insulin and lipid metabolism in liver, we hypothesized that null mutation of Ceacam1 ( Cc1 −/− ) leads to metabolic syndrome and cardiovascular abnormalities. We characterized the metabolic and cardiovascular phenotypes of six month old male Cc1 −/− mice. Cc1 −/− mice developed visceral obesity, elevated fasting plasma free fatty acids (FFA), and insulin resistance, as evidenced by fasting hyperinsulinemia and euglycemia (Table). Tail‐cuff measurements revealed higher systolic blood pressure in Cc1 −/− mice, and echocardiography of left ventricular end‐diastolic diameter (LVDd), septal (SW) and posterior (PW) wall thicknesses revealed an increased relative wall thickness (RWT; calculated as SW+PW/LVDd). No differences in systolic function were observed (data not shown). We conclude that null mutation of Ceacam1 mimics metabolic syndrome and results in elevated systolic blood pressure and left ventricular hypertrophy with preserved systolic function. This work was supported by NIH grants DK054254 (SMJ) and HC36573 (SVP).