Children born to obese mothers are known to be at an increased risk of obesity, but researchers do not fully understand why. A recent study by a research team in Brazil has found one possible reason: the umbilical cells of babies born to obese or overweight women have a modified expression of genes involved in cell metabolism and increased levels of harmful lipid molecules.
The study, “Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells,” published in the International Journal of Obesity, may improve healthcare approaches to help prevent obesity and diabetes in these children.
Environmental exposures during early development are critical determinants of disease susceptibility throughout a person’s life. Children born to women with undernutrition, obesity, or diabetes are known to have an increased risk for chronic ills such as diabetes, obesity, and cardiovascular diseases. However, the mechanisms that lead to such increased risks remain poorly understood, mostly due to the practical and ethical challenges in acquiring fetal cells.
In the study, researchers at the Universidade Federal de Pernambuco used umbilical cords, which provide an accessible infant cell source, to study fetal adaptations to maternal obesity. The team collected umbilical cords from infants born to 24 overweight or obese Brazilian women (body mass index, or BMI, of over 25 before pregnancy) and 13 women with normal BMI, and examined the endothelial cells that lined the umbilical cord vein, which carries oxygen and other nutrients from the placenta to the embryo.
“These samples give a window into the nutrients and metabolites that are coming from the mom into the infant,” Elvira Isganaitis, MD, MPH, an assistant investigator and staff pediatric endocrinologist at the Joslin Diabetes Center, and an instructor in Pediatrics at Harvard Medical School, said in a press release.
Analysis revealed that endothelial cells collected from the cords of obese women had lower levels of genes involved in the regulation of mitochondrial and lipid metabolism. Many of the differentially expressed genes had previously been linked to obesity, diabetes, or other metabolic diseases.
“This suggests that already at birth there are detectable metabolic perturbations resulting from maternal obesity,” Isganaitis said.
Analysis of fetal blood collected from the umbilical cord vein also revealed differences between obese and non-obese women. “We found that the infants of obese mothers had significantly higher levels of many lipids that are known to be metabolically deleterious, like saturated fatty acids,” Isganaitis said.
The team believes that the fat tissues from obese mothers may release lipid molecules into circulation, which eventually enter the fetal blood and may lead to altered gene expression in fetal cells.
Future studies need to confirm these changes in umbilical cells of newborns, and to assess how maternal obesity can encourage certain stem cells found in the umbilical cord to differentiate preferentially into fat cells.
The researchers hope that their work will eventually lead to the development of blood markers that detect fetuses at increased risk for obesity, allowing for tailored medical interventions that reduce such risk.
“Pregnant women engage often with their healthcare providers, and you can really tap into their motivation,” Isganaitis said. “If we could come up with tailored interventions — if we could say, take this vitamin, exercise regularly and you can minimize obesity or diabetes risk in your child — I’m sure mothers would do it.”
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