L-Leucine Improves Metabolic Disorders in Mice With in-utero Cigarette Smoke Exposure.

Yunxin Zeng,Min Huang,Hui Chen,Chenju Yi,Taida Huang,Brian G Oliver,Chunhui Sun,Nan Wang,Yi Xu,Chun Chen

doi:10.3389/fphys.2021.700246

Abstract

Objectives: Maternal cigarette smoke exposure (SE) causes intrauterine undernutrition, resulting in increased risk for metabolic disorders and type 2 diabetes in the offspring without sex differences. L-leucine supplementation has been shown to reduce body weight and improve glucose metabolism in both obese animals and humans. In this study, we aimed to determine whether postnatal L-leucine supplementation in female offspring can ameliorate the detrimental impact of maternal SE.Methods: Female Balb/c mice (6-week) were exposed to cigarette smoke (SE, 2 cigarettes/day) prior to mating for 5 weeks until the pups weaned. Sham dams were exposed to air during the same period. Half of the female offspring from the SE and SHAM dams were supplied with L-leucine via drinking water (1.5% w/w) after weaning (21-day) for 10 weeks and sacrificed at 13 weeks (adulthood).Results: Maternal SE during pregnancy resulted in smaller body weight and glucose intolerance in the offspring. L-leucine supplement in Sham offspring reduced body weight, fat mass, and fasting blood glucose levels compared with their untreated littermates; however somatic growth was not changed. L-leucine supplement in SE offspring improved glucose tolerance and reduced fat mass compared with untreated littermates.Conclusions: Postnatal L-leucine supplement could reduce fat accumulation and ameliorate glucose metabolic disorder caused by maternal SE. The application of leucine may provide a potential strategy for reducing metabolic disorders in offspring from mothers who continued to smoke during pregnancy.

Highlights

Tobacco smoking is a global public health risk
Maternal cigarette smoke exposure (SE), including direct and second-hand smoking during pregnancy, is a major cause of intrauterine undernutrition resulting in Leucine and Maternal Smoke Exposure several adverse health outcomes, including preterm birth, low birth weight, and catch-up growth in childhood (Collaco et al, 2017; Wagijo et al, 2017)
Previous studies in rodent models have shown that maternal nicotine treatment interrupts β-cell functions in offspring, and maternal SE induced intrauterine undernutrition is associated with overconsumption in offspring, increasing the risk of insulin resistance and glucose intolerance (Holloway et al, 2005; Bruin et al, 2008, 2010; Sullivan et al, 2014)

Summary

Introduction

Tobacco smoking is a global public health risk. According to the WHO, in 2016, the smoking rate in females over 15 years old was 20.7% in Europe, 12.4% in America, and 1.9% in China, while the second-hand smoking rate in females was as high as 46.9% in China (Ding et al, 2016; World Health Organization, 2019). Maternal cigarette smoke exposure (SE), including direct and second-hand smoking during pregnancy, is a major cause of intrauterine undernutrition resulting in Leucine and Maternal Smoke Exposure several adverse health outcomes, including preterm birth, low birth weight, and catch-up growth in childhood (Collaco et al, 2017; Wagijo et al, 2017) In addition to these short-term adverse effects, offspring from mothers exposed to cigarette smoke during pregnancy are more likely to develop metabolic disorders in adulthood, such as glucose intolerance, type 2 diabetes, fatty liver changes, dyslipidemia, and cardiovascular disease (Mendez et al, 2008; Gorog et al, 2011; La Merrill et al, 2015). To reduce the risk of metabolic disorder and diabetes, it is crucial to find effective preventive strategies to ameliorate the adverse impacts of maternal SE on offspring

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