As anyone who has tried to kick a pack-a-day cigarette habit can attest, nicotine is bad news. The jitters and surly attitude are bad enough, but according to a new investigation, fetal nicotine exposure also does some pretty insidious epigenetic damage. Daniel Hardy and a talented team Western University (Canada) have revealed a chromatin mechanism that explains some of the long-term consequences when nicotine is present in utero.
Hardy shares, ”We knew smoking was bad during pregnancy. But the problem is one fifth of pregnant women in Canada continue to smoke, and 30 prospective studies have shown us that that babies born to smoking mothers have a 47 per cent increase in the odds of becoming overweight. And here’s the interesting thing, that’s even after adjusting for mom’s diet and socioeconomic status.” With that public health burden in mind the Western crew searched for the epigenetic mechanisms behind these long-term environmental effects. Here’s what they found:
- Nicotine exposed male offspring had significantly elevated levels of circulating and hepatic triglycerides, elevated expression of fatty acid synthase (FAS), a crucial enzyme involved in de novo triglyceride synthesis, and increased hepatic LXRα (the nuclear receptor, Liver X receptor) protein expression, as adults.
- ChIP assays revealed a functional outcome of the altered expression; an enriched binding to a regulatory element on the FAS promoter.
- Enhanced acetylation of histone H3K9 and H3K14 was seen surrounding the FAS promoter, an sure sign of chromatin activation.
I expect we will see much more of this. As we get better tools to examine genetic expression changes, so will we see the longterm effects, not only of smoking thingsbut many other environmental exposure – such as what has happened in West Virginia.