title: Prenatal exposure to nicotine causes postnatal obesity and altered perivascular adipose tissue function.
abstract: OBJECTIVE
  Recent epidemiological studies have shown that there is an increased risk of obesity and hypertension in children born to women who smoked during pregnancy. The aim of this study was to examine the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarette smoke, on postnatal adiposity and blood vessel function.
  
  
  METHODS
  Female Wistar rats were given nicotine or saline (vehicle) during pregnancy and lactation. Postnatal growth was determined in the male offspring from weaning until 26 weeks of age. At 26 weeks of age, fat pad weight and the function of the perivascular adipose tissue (PVAT) in the thoracic aorta and mesenteric arteries were examined.
  
  
  RESULTS
  Exposure to nicotine resulted in increased postnatal body weight and fat pad weight and an increased amount of PVAT in the offspring. Contraction of the aorta induced by phenylephrine was significantly attenuated in the presence of PVAT, whereas this effect was not observed in the aortic rings from the offspring of nicotine-exposed dams. Phenylephrine-induced contraction without PVAT was not different between saline- and nicotine-exposed rats. Transfer of solution incubated with PVAT-intact aorta to PVAT-free aorta induced a marked relaxation response in the rats from saline-exposed dams, but this relaxation response was significantly impaired in the rats from nicotine-exposed dams.
  
  
  CONCLUSIONS
  Our results showed that prenatal nicotine exposure increased adiposity and caused an alteration in the modulatory function of PVAT on vascular relaxation response, thus providing insight into the mechanisms underlying the increased prevalence of obesity and hypertension in children exposed to cigarette smoke in utero.
authors.affiliation: Department of Anaesthesia (HSC-2U3), McMaster University, 1200 Main Street West, Hamilton, Ontario, Canada L8N 3Z5.
authors.forename: Yu-Jing
authors.initials: YJ
authors.lastname: Gao
authors.forename: Alison C
authors.initials: AC
authors.lastname: Holloway
authors.forename: Zhao-hua
authors.initials: ZH
authors.lastname: Zeng
authors.forename: Gareth E
authors.initials: GE
authors.lastname: Lim
authors.forename: James J
authors.initials: JJ
authors.lastname: Petrik
authors.forename: Warren G
authors.initials: WG
authors.lastname: Foster
authors.forename: Robert M K W
authors.initials: RM
authors.lastname: Lee
mesh_terms: D000273:Adipose Tissue / Q000473:pathology / Q000503:physiopathology*; D000316:Adrenergic alpha-Agonists; D000375:Aging; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology; D001808:Blood Vessels / Q000473:pathology*; D005260:Female; D006973:Hypertension / Q000209:etiology; D008297:Male; D008638:Mesenteric Arteries / Q000473:pathology; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009538:Nicotine / Q000008:administration & dosage / Q000633:toxicity*; D009765:Obesity / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D009929:Organ Size; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017208:Rats, Wistar; D015430:Weight Gain
chemical_list: D000316:Adrenergic alpha-Agonists; D009538:Nicotine