Poor nutrition during pregnancy greatly rises the offspring's risk of developing type 2 diabetes and other age-related diseases in later life.
This finding could lead to new ways of identifying people who are at a higher risk of developing these diseases and might open up targets for treatment.
AdvertisementResearchers at the University of Cambridge and the Medical Research Council (MRC) Toxicology Unit at the University of Leicester, found that, in both rats and humans, individuals who experience a poor diet in the womb are less able to store fats correctly in later life.
Storing fats in the right areas of the body is important because otherwise they can accumulate in places like the liver and muscle where they are more likely to lead to disease.
"One of the ways that our bodies cope with a rich modern western diet is by storing excess calories in fat cells. When these cells aren't able to absorb the excess then fats get deposited in other places, like the liver, where they are much more dangerous and can lead to type 2 diabetes," said Professor Anne Willis of the MRC Toxicology Unit at the University of Leicester.
The team found that a molecule called miR-483-3p controls this process. They found that miR-483-3p was produced at higher levels in individuals who had experienced a poor diet in their mother's wombs than those who were better nourished.
When pregnant rats were fed low protein diets their offspring had higher levels of miR-483-3p. This led to them developing smaller fat cells and left them less able to store fats in adulthood.
These rats were less likely to get fat when fed a high calorie diet but were at a higher risk of developing diabetes. And the team also found that miR-483-3p was present in elevated levels in a group of people who were born with a low birth weight.
The researchers found that miR-483-3p works by suppressing a protein called GDF3. When they studied a group of adult humans who were born with a low birth weight, they found that GDF3 protein was present at around only thirty percent of the levels found in people born at a normal weight.
The finding has been just published in the journal Cell Death and Differentiation.
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