Fetal exposure to bisphenol A disrupts the body's endocrine system
Updated: Mar 28, 2019
Bisphenol A, commonly known as BPA, is a chemical compound usually found in food containers. Recently, various experts have expressed concern over its safety. A new mouse study suggests that prenatal exposure to BPA may increase the offspring's risk of obesity by disrupting the body's endocrine system.
A new study of mice shows that prenatal exposure to BPA may lead to obesity in the offspring.
Bisphenol A (BPA) is a compound that was approved by the United States Food and Drug Administration (FDA) in the 1960s.
A health study carried out by the Centers for Disease Control and Prevention (CDC) detected BPA in as much as 93 percent of more than 2,500 urine samples. Because the substance is found in the vast majority of food containers, and because humans are exposed to it on such a wide scale, the National Toxicology Program (NTP) decided to evaluate it in 2010.
After a careful toxicological and endocrinological assessment, the NTP expressed "some concern" over the possibility that BPA may affect the development of fetuses, infants, and children. "Some concern" is the middle point of a five-point scale used by the NTP.
One way that BPA can be harmful is by disrupting the body's endocrine system, imitating the female sex hormone estrogen.
A new study, published in the journal Endocrinology, suggests that prenatal exposure to BPA, or synthetic estrogen, may increase the risk of obesity in the offspring by altering the body's appetite control system.
Researchers led by Alfonso Abizaid, Ph.D., from the Department of Neuroscience at Carleton University in Ottawa, Canada, fed pregnant mice BPA with their food, therefore exposing the fetuses to lower levels of the chemical than what was deemed safe by the FDA.
As soon as the offspring were born, Abizaid and colleagues administered the newborns injections of leptin. Leptin is often referred to as the satiety hormone, because it sends signals to the brain to let it know if the body needs energy - namely, food. Leptin regulates the appetite and is directly connected to the amount of body fat. When a person amasses body fat, the leptin levels increase, telling the hypothalamus to lower the appetite as the body can take its energy from the fat it already has.
Dysfunctions in the body's way of processing leptin are linked to obesity. For instance, when the body is obese, the individual also develops something called leptin resistance, which is a lack of sensitivity to the increased levels of the hormone in the body.
In this study, after injecting the mice's offspring with leptin, the researchers analyzed the rodents' brain tissue and their blood to see how they responded to the hormone.
A control group of mice was either not exposed to the chemical, or they received diethylstilbestrol (DES) - a synthetic form of estrogen commonly used in rodent models of human intrauterine exposure. Here, DES was used in the parents so that their babies could be compared to those born to BPA-exposed mothers.
All of the mice were put on the same control diet to eliminate any potential differences in nutrition.
BPA disrupts the body's appetite-regulating mechanism
Healthy newborns normally display a surge in leptin when they are 8 days old. This forms the hypothalamic circuits that respond to satiety cues.
In prenatally BPA-exposed rodents, however, this surge occurred 2 days late. The mice exposed to DES did not have the surge at all. Additionally, BPA-exposed mice had lower fiber density and exhibited reduced brain activity in the hypothalamic circuits dealing with energy expenditure and appetite control.
Furthermore, when the mice were administered leptin, control mice that had not been exposed to BPA or DES lost more weight than their BPA and DES-free counterparts.
"Our findings show that bisphenol A can promote obesity in mice by altering the hypothalamic circuits in the brain that regulate feeding behavior and energy balance," explains the study's senior author. "Low-level prenatal exposure to BPA delays a surge of leptin after birth that allows mice to develop the proper response to the hormone. BPA exposure permanently alters the neurobiology in the affected mice, making them prone to obesity as adults."
Abizaid also expresses concern over the effect BPA can have on obesity and metabolic disease:
"This study improves our understanding of how BPA can disrupt the endocrine system in a manner that raises the risk of obesity in animals. Since BPA has also been linked to obesity in humans, people need to be aware that environmental factors can lead to increased susceptibility to obesity and cardio-metabolic disorders."