Posted on Dec 03, 2018, 7 p.m.
Smoking during pregnancy is recognized to increase risks such as low birth weight and being born premature, recent studies from the University of Kentucky suggest maternal smoking is linked to offspring obesity via epigenetic control of adipokine, as published in the Experimental Physiology.
Maternal smoking increases levels of chemerin proteins which is linked to obesity in adults and now in newborn babies with an impact on epigenetic control of chemerin which then increases risks of obesity later in life. The research provides a potential novel mechanism behind increased later life risk of obesity in offspring born exposed to maternal smoking.
35% of adults and 20% of children are obese in the USA, costing an estimated 200 billion a year; and 26% of adults and 20% of children are obese in the UK, costing an estimated 27 billion a year. Environmental factors other than exercise, diet, and genetics are suggested to be at play as these rates continue to rise; multiple factors have parts in development of metabolic disorders and obesity, one potential contribution is from the in utero environment during pregnancy.
Chemerin is an adipokine that regulates fat cell differentiation, chemokine levels are elevated in those who are obese and are exposed to smoke. Whether levels are altered in neonates exposed to cigarette smoke in utero has hasn’t been investigated, prompting this study.
Chemerin gene expression was examined in discarded foreskin samples from circumcised infants born from smoking mothers and compared to those from non-smoking mothers: analyses showed chemerin expression was significantly higher from those exposed to smoking in utero; and levels were also increased in smoking exposed foreskin derived primary dermal fibroblast grown in culture using adipogenic cocktails.
Additional analyses showed chemerin DNA methylation was lower in whole tissues from newborns exposed to smoking in utero, suggesting epigenetic mechanisms may be involved in smoke induced changes to chemerin gene expression. The researchers concluded that present data supports a potential mechanism whereby those exposed to smoking in utero could demonstrate greater rates of obesity later in life.
Limitations to the study were acknowledged such as results can’t be extrapolated to female offspring; and measurements were made in epidermal/dermal samples predicting that the adipose tissues would respond in similar fashion but may not be the case. They were only able to assess DNA methylation and mRNA expression of chemerin do to limited tissue availability rather than protein expression, and recommend this should be investigated. Even with the limitations the researchers are confident in their results providing important evidence of a link between maternal smoking and increased chemerin mRNA expression.
The researchers long term plan is to study impacts of exercise during pregnancy and possibility to improve outcomes in offspring; and in the future working on ways to improve smoking cessation programs and increasing exercise as a way to combat negative outcomes in offspring.
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