| Prenatal Exposure to Cigarette Smoke Induces Diet- and Sex‑Dependent Dyslipidemia and Weight Gain in Adult Murine Offspring Sheung P. Ng,1 Daniel J. Conklin,2 Aruni Bhatnagar,2 Duane D. Bolanowski,2 Jessica Lyon,1 and Judith T. Zelikoff1 1New York University School of Medicine, Nelson Institute of Environmental Medicine, Tuxedo, New York, USA; 2University of Louisville, Institute of Molecular Cardiology, Louisville, Kentucky, USA Abstract
Background: Cardiovascular disease (CVD) affects 71 million American adults and remains the leading cause of death in the United States and Europe. Despite studies that suggest that the development of CVD may be linked to intrauterine growth or early events in childhood, little direct experimental evidence supports the notion. Objective: We investigated whether exposure to cigarette smoke in utero alters the risk of developing CVD later in life. Methods: We exposed B6C3F1 mice (via whole-body inhalation) to either filtered air or mainstream cigarette smoke (MCS, at a particle concentration of 15 mg/m3) from gestational day 4 to parturition. Adult offspring were fed a normal chow diet or switched to a high-fat diet 2 weeks before sacrifice. We measured dam and offspring body weight, plasma lipid parameters, lipoprotein subclass particle numbers and sizes, and total antioxidant capacities. Results: Adult female mice prenatally exposed to MCS demonstrated significantly higher body weight and levels of plasma high-density lipoprotein (HDL) and low-density lipoprotein than did their air-exposed counterparts. When fed a high-fat diet for 2 weeks, males, but not females, exposed prenatally to MCS gained substantially more weight and exhibited dramatic alterations in total cholesterol and HDL levels compared with their air-exposed counterparts. Conclusions: These data provide, for the first time, direct experimental evidence supporting the notion that prenatal exposure to cigarette smoke affects offspring weight gain and induces a lipid profile that could alter the offspring’s risk of developing CVD later in life. Key words: cardiovascular disease, cigarette smoke, dyslipidemia, fetal basis of adult disease, fetal insult, prenatal exposure, weight gain. Environ Health Perspect 117:1042–1048 (2009) . doi:10.1289/ehp.0800193 available via http://dx.doi.org/ [Online 13 April 2009]
Address correspondence to J.T. Zelikoff, New York University School of Medicine, Nelson Institute of Environmental Medicine, 57 Old Forge Rd., Tuxedo, NY 10987 USA. Telephone: (845) 731-3528. Fax: (845) 351-5472. E-mail: Judith.Zelikoff@nyumc.org This work was supported in part by the National Institute of Environmental Health Sciences (NIEHS) Center Pilot Project (5 P30 ES00260-44) , Institute for Science and Health (07-1500-01RFA05) , NIEHS P30 ES11860 (A.B.) , and a grant from Phillip Morris (A.B.) . This study was supported in part by Philip Morris. Other research studies performed by J.T.Z.’s laboratory have been supported in part by Philip Morris USA Inc. and Philip Morris International. Received 16 September 2008 ; accepted 20 March 2009.
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