A bit of a correction artemis, all groups were allowed to eat as much as they wanted. Substitution of saturated fat with unsaturated fats resulted in the animals both eating less and losing weight. At least some of the weight loss was due to the decreased consumption. It also reversed the insulin resistance, improved glucose control, and reversed the inflammation in the hypothalamus. Injecting the omega 3 and 9 fatty acids directly into the cerebral hemispheres also resulted in decreased intake, reversed hypothalamic inflammation and resulted in the hypothalamus being more responsive to leptin thereby sending signals out to burn more (“pro-thermogenic signaling”). Thus some weight loss was presumably due to changes in metabolism in addition to the decrease in intake. And the peripheral effects were at least somewhat, if not primarily, due to central effects.
But yes different sources of nutrition have very different effects on different brains and the brain effects seem to lead the show in the development of and the defense of obesity. Some brains are more likely to respond to various environmental triggers with inflammation or with various receptor and functional changes than others. The various developing brains in utero, with their own genetic predispositions, respond to the nutrition that gets to them across the placenta and are, as a result, more or less likely to react to later environmental triggers in different ways.
To me this is fascinating stuff. Pertinent to the op’s premise- Yes placental insufficiency and fetal undernutrition is both correlated with risk for obesity and with increased risk for metabolic syndrome even if not overweight or obese. (Yes, Taomist, your brother is at relative increased risk for developing metabolic syndrome even with a normal BMI. The good news: increased risk does not mean destiny.) One suspects that such is mediated by these central effects. And yes a maternal diet relatively low in unsaturated fats while high in (?certain?) saturated fats (?and other substances?) will cause central hypothalamic damage that is associated with later risk for both obesity and metabolic syndrome, at least in the animal model. Thus it is not the fat mother to be, but the food that the mother to be eats which is of course correlated with her being overweight or obese herself. Of course if she eats little enough of it she won’t be clinically obese (see our often mentioned professor on his Twinkie diet), but the damage to her baby and to her own hypothalamus, and thus the future long term risks to both of them, are still incurred.
The story gets even more interesting because there are multiple receptor networks involved with both various tissue and various CNS locations, each of which may respond to various stimuli differently …
Those who are not interested in the unfolding of the science explaining how the genetic predisposition to obesity is impacted by our current nutrition and who want to keep their understanding limited to thinking that the 1/3rd of the adult population of Americans who are neither overweight or obese are just more disciplined than the other 2/3rds of the population, that reciting “just move more and eat less” is the whole story, are welcome to their ways. But IMHO they are missing out on some very exciting emerging science.
My interest, beyond the thrill of seeing scientific understanding unfold, is learning how to prevent obesity. Prenatal nutrition is part of the story. Altering the horrible nutritional and activity milieus that kids grow up in in our society by working at multiple levels is part of it as well.
MsRobyn I completely agree.