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Prenatal exposure to nicotine causes postnatal obesity and altered perivascular adipose tissue function
Yu-Jing Gao1, Alison C Holloway, Zhao-hua Zeng
1Department of Anaesthesia (HSC-2U3), McMaster University, 1200 Main Street West, Hamilton, Ontario, Canada L8N 3Z5.
Insights
Prenatal nicotine exposure in rats led to increased offspring adiposity and impaired blood vessel function. This study reveals mechanisms linking maternal smoking during pregnancy to childhood obesity and hypertension.
Area of Science:
- Reproductive Biology
- Cardiovascular Physiology
- Developmental Toxicology
Background:
- Maternal smoking during pregnancy is linked to increased childhood obesity and hypertension.
- Nicotine, a primary component of cigarette smoke, is suspected to mediate these adverse effects.
- Understanding nicotine's impact on fetal development is crucial for public health.
Purpose of the Study:
- To investigate the effects of fetal and neonatal nicotine exposure on postnatal adiposity.
- To examine the impact of nicotine on blood vessel function in offspring.
- To elucidate the mechanisms behind increased obesity and hypertension risks associated with in utero smoke exposure.
Main Methods:
- Wistar rats received nicotine or saline during pregnancy and lactation.
- Male offspring were monitored for growth from weaning to 26 weeks.
- Fat pad weight and perivascular adipose tissue (PVAT) function in aorta and mesenteric arteries were assessed.
Main Results:
- Nicotine exposure increased offspring body weight and fat pad weight.
- Perivascular adipose tissue (PVAT) function was altered, impairing vascular relaxation.
- Nicotine exposure affected the modulatory role of PVAT on phenylephrine-induced aortic contraction.
Conclusions:
- Prenatal nicotine exposure promotes adiposity in offspring.
- Nicotine exposure alters PVAT's modulatory function on vascular responses.
- These findings offer insights into the developmental origins of obesity and hypertension linked to maternal smoking.
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.
Research Methods And Procedures:
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.
Discussion:
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.
