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Effect of Nicotine Exposure During Pregnancy and Lactation on Maternal, Fetal, and Postnatal Rat IGF-II Profile

Division Maternal-Fetal Medicine, Department OBS-GYN and Newborn Care, The Ottawa Hospital University of Ottawa, Ontario, Canada, Chronic Disease Program, Ottawa Health Research Institute, Ottawa, Ontario, Canada, agruslin{at}ottawahospital.on.ca

Carolyn E. Cesta, BSc

Reproductive Biology Division, Department of Obstetrics & Gynecology, McMaster University, Hamilton, Ontario, Canada

Michael Bell, BSc

Chronic Disease Program, Ottawa Health Research Institute, Ottawa, Ontario, Canada

Qing Qiu, MD

Chronic Disease Program, Ottawa Health Research Institute, Ottawa, Ontario, Canada

Maria A. Petre, BSc

Reproductive Biology Division, Department of Obstetrics & Gynecology, McMaster University, Hamilton, Ontario, Canada

Alison C. Holloway, PhD

Reproductive Biology Division, Department of Obstetrics & Gynecology, McMaster University, Hamilton, Ontario, Canada

Smoking during pregnancy has been shown to result in an increased risk of low birth weight. However, the mechanisms underlying this association are poorly understood. The insulin-like growth factor (IGF) system plays a critical role in the regulation of feto-placental growth and development, and abnormal processing of proIGF-II may alter its biological function. Our goal was to investigate the effects of exposure to nicotine on maternal, fetal, and neonatal IGF-II processing. Nulliparous female Wistar rats were randomly assigned to receive saline (vehicle) or nicotine bitartrate (1 mg·kg^—1·d^{— 1}). After mating, dams were euthanized at embryonic days 15, 18, and 21, and fetal body weight was recorded. Serum (fetal and maternal) was collected for determination of the IGF-II profile by Western blot analysis. Nicotine exposure prevented the decrease in maternal IGF-II processing seen in controls with advancing gestation. However, there was no influence of nicotine on fetal levels of IGF-II. Postnatally (postnatal day [PND] 21), pups exposed to nicotine in utero had decreased levels of big IGF-II. Our results show, for the first time, that nicotine exposure prevents the decrease of IGF-II processing in the maternal compartment. This may represent a compensatory mechanism allowing the mother to counteract the negative influence of nicotine on fetal growth and development. Our postnatal findings of suppressed IGF-II may help explain some of the long-term health complications seen in individuals exposed to smoking in utero.

Key Words: Nicotine • insulin-like growth factor-II • pregnancy • fetal growth restriction.

This version was published on September 1, 2009

Reproductive Sciences, Vol. 16, No. 9, 875-882 (2009)
DOI: 10.1177/1933719109337038


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