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In Utero Exposure To Cigarette Smoke Promotes Cardiac Dysfunction In High‐fat Fed Mice
Author(s) -
Xia Huijing,
Rodrigues Samya Lima,
Ronis Martin J.,
Noel Alexandra,
Penn Arthur,
Pullium Casey,
Gardner Jason,
Varner Kurt J.
Publication year - 2018
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.2018.32.1_supplement.604.5
Subject(s) - offspring , in utero , medicine , cardiac function curve , smoke , diastole , endocrinology , passive smoking , tobacco smoke , pregnancy , nicotine , cardiology , fetus , heart failure , biology , chemistry , pathology , blood pressure , genetics , environmental health , organic chemistry
Maternal smoking during pregnancy is associated with an increased risk for metabolic syndrome, a risk factor for heart disease. In this study, we investigated whether in utero exposure to second hand cigarette smoke would adversely affect cardiac structure/function in the exposed offspring fed a high‐fat diet. Pregnant mice (C57B1/6J) were exposed to cigarette smoke or air (4 hr/d) on gestational days 6–19. The male offspring (age: 35 days) from the smoke and air exposure groups were fed either normal chow, or high‐fat liquid diet (35% of fat; HFD) for 16 weeks (n=12/group). Cardiac function was measured by echocardiography at baseline (30 days) and at the end of pair feeding. Mice were then sacrificed and heart tissue collected for histological analysis. At baseline, left ventricular internal diameter at end systole was significantly greater in the smoke‐exposed compared to the air group (3.2±0.1 vs 2.8±0.1 mm, P<0.05). All other baseline echocardiographic parameters were similar between the groups. 16 weeks of HFD feeding significantly increased the body weight and heart weight/tibial length in both the air and smoke‐exposed mice (P<0.05, smoking+HFD vs. smoking+chow; air+HFD vs. air+chow). However, there was no significant difference in body weight or heart weigh/tibial length between the smoking+HFD and air+HFD groups. Compared to air+HFD mice, smoking+HFD mice had significantly decreased left ventricular internal diameters and volumes during diastole (3.95±0.09 vs. 4.34±0.24 mm; 67.8±1.5 vs. 85.4±4.4 μl, P<0.05) and systole (2.91±0.07 vs. 3.34±0.15 mm; 32.5±1.9 vs. 46.3±5.1 μl, P<0.05), accompanied by increases in left ventricular wall during diastole (0.72±0.03 vs. 0.66±0.03 mm, P<0.01) and septal thickness during systole (1.2±0.06 vs. 0.99±0.05 mm, P<0.05) and increased fractional shortening. There was also increased collagen in the hearts of the smoking+HFD mice. These data indicate the development of concentric cardiac hypertrophy in smoking+HFD mice. We conclude that in utero exposure to second hand cigarette smoke produces differential cardiac responses following challenge with obesogenic high fat diet. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .