The adage “You are what you eat” should be rephrased to include “and so are your children,” based on metabolic research pioneered by researchers at UB.
Previous studies by these UB scientists showed that rat pups raised artificially on a high-carbohydrate milk formula identical in calories to mother’s milk developed changes in pancreatic islets, resulting in overproduction of insulin and obesity in adulthood. Now the researchers have shown that this metabolic “malprogramming” is permanent and occurs in utero, resulting in the next-generation rats born to HC mothers carrying the HC phenotype. Rat fetuses had increased plasma insulin levels, increased mRNA levels of preproinsulin, a precursor of insulin, and increased insulin in the pancreas, without an increase in body weight, plasma glucose level or a change in islet structure. They also found changes in the hypothalamus, the brain’s center of appetite regulation, that result in appetite stimulation.
These studies were done with rats, but Mulchand Patel, UB distinguished professor of biochemistry and first author on the study, speculated that there is good reason to think the mechanism could be similar in humans.
“Obesity can be perpetuated via the maternal intrauterine environment,” says Patel. “Our earlier studies looked at progeny in the post-weaning period, so we didn’t know how early this malprogramming occurred. Now we know it occurs in utero. We predicted that this could be the case, and our present findings support this prediction.”
The research was supported by grants from the National Institutes of Health.