Modulation of neural regulators of energy homeostasis, and of inflammation, in the pups of mice exposed to e-cigarettes

Hui Chen,Gerard Li,Yik Lung Chan,Tara Nguyen,David Van Reyk,Sonia Saad,Brian G Oliver

doi:10.1016/j.neulet.2018.07.001

Abstract

BackgroundMaternal smoking can lead to perturbations in central metabolic regulators such as neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) signalling components in offspring. With the growing interest in e-cigarettes as a tobacco replacement, this short report assessed central metabolic regulation in offspring of mouse dams exposed to e-cigarettes. We examined the impact of continuous use of e-cigarettes, and e-cigarette replacement of tobacco cigarettes during pregnancy. Supplementation of an antioxidant l-carnitine was also co-used with tobacco cigarette in the mother to determine whether the impact of maternal tobacco smoking was oxidative stress driven. MethodsBalb/c mice were exposed to either nicotine-containing (E-cig18) or nicotine-free (E-cig0) e-cigarette aerosols or tobacco smoke (SE) prior to mating and until their pups were weaned. After mating, two SE sub-groups were changed to E-cig18 exposure (Replacement), or supplementation l-carnitine while SE was continued. Male offspring were studied at weaning age. ResultsThe offspring of E-cig0 dams were the heaviest with the most body fat. Replacing SE with E-cig18 during pregnancy resulted in offspring with significantly less body fat. E-cig0 offspring had significantly increased mRNA expression of brain NPY and iNOS. Maternal SE upregulated mRNA expression of NPY, NPY Y1 receptor, POMC downstream components, and iNOS expression, which were normalised in Replacement offspring, but only partially normalised with maternal L-carnitine supplementation during gestation and lactation. ConclusionsMaternal exposure to either tobacco and nicotine-free e-cigarettes lead to disturbances in the level of central homeostatic control markers in offspring, suggesting that maternal exposure to e-cigarettes is not without risks.

Highlights

The brain plays an important role in energy metabolic homeostasis, while studies have demonstrated that maternal smoking can disturb such regulation in the offspring
The first major finding of this study is that maternal exposure to nicotine-free e-vapor induces significant adiposity, dysregulation of brain metabolic regulatory pathways and increased inducible nitric oxide synthases (iNOS) expression suggesting that maternal e-vapor exposure is not necessarily risk-free
The second major finding is that replacement of tobacco smoke with e-vapour normalised the effects of tobacco smoke upon the same regulatory pathways, which is comparable and superior to the supplementation with the antioxidant L-carnitine during gestation and lactation

Summary

Introduction

The brain plays an important role in energy metabolic homeostasis, while studies have demonstrated that maternal smoking can disturb such regulation in the offspring. The offspring of such mothers may undergo nicotine withdrawal by reducing milk intake and increasing solid food consumption, which can have an impact upon feeding behaviour and energy homeostasis, resulting in increased risk of obesity later in life [16]. Maternal smoking can lead to perturbations in central metabolic regulators such as neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) signalling components in offspring. Conclusions: Maternal exposure to either tobacco and nicotine-free e-cigarettes lead to disturbances in the level of central homeostatic control markers in offspring, suggesting that maternal exposure to e-cigarettes is not without risks.

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