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In-Bred Obesity Resistance Can Be Cancelled Out By Perinatal High-Fat Diet

sharma-obesity-running-mouseThe periods of early development both in utero and shortly after birth appear to be critical periods for epigenetic programming of lifelong obesity risk.

This is once again demonstrated in a fascinating series of experiments by Stefano Guidotti and colleagues from the University of Groningen, The Netherlands, in a paper published in Physiology and Behaviour.

The researchers performed their experiments in mice that were selectively bred over 50 generations to voluntarily spend hours in running wheels. Interestingly, the female “runner” mice remain resistant to becoming obese as adults when exposed to a high-fat diet even when they don’t have access to a running wheel.

Thus, these mice are resistant to developing obesity whether they run or just sit around.

What the researchers now show is that this “resistance” to gaining excess weight (bred over generations) can be fully cancelled out simply by exposing the mice to a high-fat diet for a couple of days shortly after birth.

With this exposure, these mice (and even their offspring) are suddenly no longer resistant to weight gain later in life and in fact gain as much weight on high-calories diets as normal mice.

Even more interestingly, the short term perinatal exposure to the high-energy diet does not cancel out their love for running. When given a wheel, they continue running just as much as before but even this no longer prevents them from gaining weight.

Thus it appears that exposure to a high-energy diet during the perinatal period can have profound effects on the risk of developing adult obesity even in animals bred to be obesity resistant – and, the love for running, does not appear to protect against weight gain.

Or, as the authors put it,

“..resistance to high-energy diet-induce obesity in adult female mice from lines selectively bred over ~ 50 generations for increased wheel running behavior was blocked by additional perinatal high-energy diet exposure in only one cycle of breeding. An explanation for this effect is that potential allelic variants underlying the trait of diet-induced obesity proneness were not eliminated but rather silenced by the selection protocol, and switched on again by perinatal high-energy diet exposure by epigenetic mechanisms”

Moreover, this effect of perinatal high-energy diet exposure and its “reversal effect” on obesity resistance can be passed on to the next generation.

Reason enough to wonder just how much the rather dramatic changes in perinatal feeding of infants over the last few decades may be contributing to the obesity epidemic.

Edmonton, AB

1 Comment

  1. You say you “wonder” whether perinatal diets in the last few decades have contributed to the obesity epidemic…I would say that this is just more evidence that in fact that we are jsut starting to understand all the impacts of the the “experiments” conducted by the use of artificial baby milks.

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