Medical school identifies placental protein as possible birthweight regulator

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New findings from the University of Minnesota Medical School are helping to understand why some people are more likely to be overweight and develop type 2 diabetes – and that starts in the womb.

Previous association studies have shown that low birth weight in infants is a powerful determinant of possible obesity and type 2 diabetes. The placenta of low birth weight infants has a reduced level of mTOR (mechanistic target of rapamycin) and the placenta of larger infants has an increased level of mTOR. Building on this research, a U of M Medical School study published in JCI Insight is the first to directly implicate mTOR, a nutrient sensing protein in the placenta, as a potential regulator of an infant’s birth weight.

“It is clear from human and preclinical studies that type 2 diabetes is fetal in origin, but we do not yet understand the mechanisms by which this programming of metabolic disorders or type 2 diabetes occurs,” said Emilyn Alejandro, Ph.D. , Associate Professor at the Institute for Integrative Biology and Physiology. “Our study is the first to show a direct role for a placental protein like mTOR.”

They found that in preclinical studies:

  • After elimination of mTOR in the placenta, female offspring had lower birth weights and an increased risk of obesity and insulin resistance in adulthood.
  • In contrast, after an increase in mTOR signaling in the placenta, female adult offspring were protected from obesity caused by a high-fat diet.

“A causal relationship between placental mTOR and the metabolic health of the offspring has not been tested, and our study suggests that the manipulation of mTOR in the placenta is sufficient to have a permanent and lasting impact on the health of the offspring,” said Brian Akhaphong, lead author and post graduate intern at the Alejandro Lab. “Our hope is that we can identify proteins that we can therapeutically target through maternal health to reduce the prevalence of type 2 diabetes.”

The research team will continue their study and investigate which metabolic tissues of the offspring are permanently affected by placental mTOR signaling. Megan Beetch, Ph.D., a postdoctoral fellow, will study epigenetics, or hereditary changes in gene expression that do not involve changes in the underlying DNA sequence.

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More information:
Brian Akhaphong et al., Placental mTOR-Complex1 Regulates Fetal Obesity and Insulin Resistance Programming in Mice, JCI Insight (2021). DOI: 10.1172 / jci.insight.149271 Provided by the University of Minnesota Medical School

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