Obesity and type 2 diabetes in pregnancy can program children to develop metabolic problems in life, but if the children are careful about what they eat, it can be overturned according to new Australian research.
The study, from the Victor Chang Cardiac Research Institute, is published in the June edition of the journal, Epigenetics. Lead author, Associate Professor Cath Suter, says little has been understood until now about how being overweight in pregnancy impacts on the future health of children.
“We already know that if mothers are undernourished during pregnancy, their children are born small and are more likely to develop obesity and other problems later in life. But lack of nutrition isn’t a problem in modern‐day Western society. The big problem now is over‐nutrition,” says A/Professor Suter.
By using genetically identical mice as a model, the team investigated the effects of having a mother with obesity and type 2 diabetes.
“It’s difficult for us to study this in human populations, because there are so many differences in postnatal lifestyles and genetic variations. So we studied a strain of mice where some develop obesity quite naturally. Basically they eat too much and get fat, which mimics the Western population fairly well,” said A/Professor Suter.
The research team found that the offspring of obese and diabetic mothers were predisposed to developing metabolic disease, and that males were particularly affected. These offspring were heavier than the offspring of lean mothers, even as babies, and when weaned onto a Western‐style ‘junk food’ diet, they developed the hallmarks of type 2 diabetes within a few weeks.
After two months, they had developed severe fatty liver disease. The offspring of lean mothers remained normal on the same Western diet.
But the news isn’t all bad. The offspring of obese mothers, while heavier and fatter, could be protected from overt metabolic disease and fatty liver by sticking to a low‐fat diet.
“This study provides hope that we can break the current cycle of obesity, and that metabolic syndrome may not be a fait accompli,” said Dr Jennifer Cropley, co‐author on the paper. “Children of overweight mothers might have to be much more careful about what they eat, but if they are, they can avoid overt disease, and in turn avoid programming their own children to be prone to metabolic disease.”
The team of researchers found that the predisposed mice had widespread ‘epigenetic’ changes across their genome. Epigenetics is an emerging research area that looks at the way that our genes ‘behave’ ‐that is, whether they are switched ‘on’ or ‘off’.
“We know that epigenetic marks laid down in the womb are fairly stable throughout our lifetime,” said Dr Cropley. “Our findings suggest that if the laying down of these marks is interfered with by for example, poor maternal nutrition, the outcome can be an increase in disease risk in adulthood.”
A/Professor Suter says that the dramatic rise in obesity in the last 30 years cannot be blamed solely on our genetics.
“Our grandparents’ generation was mostly slim and healthy – there just hasn’t been enough time for our genes to have changed that much. But epigenetics is more plastic, and can respond to environmental cues.”
Suter and Cropley suspect that many modern day complex diseases may have an epigenetic, rather than genetic, basis.
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