AIMS/HYPOTHESIS: Epidemiological studies report an increased risk of obesity and type 2 diabetes in children born to women who smoked during pregnancy. This study examines the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarettes, on postnatal growth, adiposity and glucose homeostasis. METHODS: Female Wistar rats were given either saline (vehicle) or nicotine (1 mg kg(-1) day(-1)) during pregnancy and lactation. Serum and pancreas tissue were collected from the infant rats at birth. Postnatal growth was assessed weekly until the rats reached 26 weeks of age and glucose homeostasis was examined by OGTTs performed at 7 and 26 weeks of age. RESULTS: Exposure to nicotine resulted in increased postnatal growth and adiposity. Nicotine exposure also resulted in dysglycaemia at 7 and 26 weeks of age. Serum insulin concentrations were decreased in the pups exposed to nicotine at birth. This was associated with increased beta cell apoptosis (pups of saline-treated mothers 8.8+/-1.21% apoptotic beta cells; pups of nicotine-treated mothers 27.8+/-3.1% apoptotic beta cells). CONCLUSIONS/ INTERPRETATION: Fetal and neonatal exposure to nicotine results in metabolic changes in the offspring that are consistent with obesity and type 2 diabetes. We propose that these metabolic changes may be a consequence of the initial insult to the beta cell during fetal life and that this animal model has many characteristics of diabetes in humans.
AIMS/HYPOTHESIS: Epidemiological studies report an increased risk of obesity and type 2 diabetes in children born to women who smoked during pregnancy. This study examines the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarettes, on postnatal growth, adiposity and glucose homeostasis. METHODS: Female Wistar rats were given either saline (vehicle) or nicotine (1 mg kg(-1) day(-1)) during pregnancy and lactation. Serum and pancreas tissue were collected from the infantrats at birth. Postnatal growth was assessed weekly until the rats reached 26 weeks of age and glucose homeostasis was examined by OGTTs performed at 7 and 26 weeks of age. RESULTS: Exposure to nicotine resulted in increased postnatal growth and adiposity. Nicotine exposure also resulted in dysglycaemia at 7 and 26 weeks of age. Serum insulin concentrations were decreased in the pups exposed to nicotine at birth. This was associated with increased beta cell apoptosis (pups of saline-treated mothers 8.8+/-1.21% apoptotic beta cells; pups of nicotine-treated mothers 27.8+/-3.1% apoptotic beta cells). CONCLUSIONS/ INTERPRETATION: Fetal and neonatal exposure to nicotine results in metabolic changes in the offspring that are consistent with obesity and type 2 diabetes. We propose that these metabolic changes may be a consequence of the initial insult to the beta cell during fetal life and that this animal model has many characteristics of diabetes in humans.
Authors: Alina L Micu; Sharon Miksys; Edward M Sellers; Dennis R Koop; Rachel F Tyndale Journal: J Pharmacol Exp Ther Date: 2003-05-15 Impact factor: 4.030
Authors: G J Wetscher; M Bagchi; D Bagchi; G Perdikis; P R Hinder; K Glaser; R A Hinder Journal: Free Radic Biol Med Date: 1995-05 Impact factor: 7.376
Authors: Alison C Holloway; Donald Q Cuu; Katherine M Morrison; Hertzel C Gerstein; Mark A Tarnopolsky Journal: Endocrine Date: 2007-06 Impact factor: 3.633
Authors: Melissa A Suter; Adi R Abramovici; Emily Griffin; D Ware Branch; Robert H Lane; Joan Mastrobattista; Virender K Rehan; Kjersti Aagaard Journal: Birth Defects Res A Clin Mol Teratol Date: 2015-07-14
Authors: Wei Bao; Karin B Michels; Deirdre K Tobias; Shanshan Li; Jorge E Chavarro; Audrey J Gaskins; Allan A Vaag; Frank B Hu; Cuilin Zhang Journal: Int J Epidemiol Date: 2016-01-09 Impact factor: 7.196