Obese pregnant women often give birth the babies at risk of the disease.
As obesity rates for pregnant women continue to climb, scientists at the University of Colorado Anschutz Medical Campus have discovered that increasing a specific hormone during pregnancy can reduce or eliminate the chances that the baby will become obese as well.
“In the U.S., nearly two-thirds of women enter pregnancy either overweight or obese,” said the study’s senior author Professor Thomas Jansson, MD, PhD at the CU School of Medicine. “That makes them susceptible to gestational diabetes, preterm labor and preeclampsia. At the same time, the baby is often born larger with more fat than normal.”
The infants often go on to become obese as well, setting up a vicious cycle that drives the epidemic, Jansson said.
So he and his research team set out to find interventions that might stop that cycle, focusing on the hormone Adiponectin which makes people sensitive to insulin. High levels of the hormone guard against obesity and diabetes, while low levels put people at risk for the diseases.
Adiponectin acts as a brake on the amount of nutrients passed between a pregnant woman and her fetus through the placenta. Low levels of the hormone release the brake resulting in a larger than normal baby with more body fat.
The researchers infused obese, pregnant mice with Adiponectin during the last four days of their 20-day gestational periods, effectively normalizing the levels of the hormone in their bodies.
“It completely reversed all the negative effects on the placenta,” Jansson said. “The pups of the obese mice had completely normal weights. Their glucose levels were also normal. We were able to preempt all the usual negative consequences of these kinds of pregnancies.”
This is the first time, he said, that such an experiment has been done.
“This hormone or a similar agent could feasibly do the same thing for humans that it did for mice,” Jansson said. Another group of researchers has developed a compound similar to Adiponectin that can be taken orally and is now in clinical trials.
Jansson said more work needs to be done to track the long-term effects of the hormone treatment on the mice.
“But we have laid the foundation for what we believe might ultimately help break the cycle of obesity that has approached epidemic proportions in our society,” Jansson said.
About this neuroscience research
The study was published Monday in the Proceedings of the National Academy of Sciences. The co-authors include, Fredrick J. Rosario, PhD, instructor at CU Anschutz, Professor Theresa Powell, PhD, of CU Anschutz and Irving L. M. Aye of Cambridge University in England.
Source: David Kelly – UC Anschutz Image Source: The image is in the public domain Original Research: Full open access research for “Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth” by Irving L. M. H. Aye, Fredrick J. Rosario, Theresa L. Powell, and Thomas Jansson in PNAS. Published online September 28 2015 doi:10.1073/pnas.1515484112
Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth
Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity.
“Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth” by Irving L. M. H. Aye, Fredrick J. Rosario, Theresa L. Powell, and Thomas Jansson in PNAS. Published online September 28 2015 doi:10.1073/pnas.1515484112