The new study found mice born to mothers exposed to bisphenol A (BPA) were less responsive to the satiety hormone leptin.
Its effect on her offspring suggests that BPA may exert its effects by redefining the developmental programming of certain brain regions.
“Our findings show that bisphenol A can promote obesity in mice by altering the hypothalamic circuits in the brain that regulate feeding behaviour and energy balance," said the study's senior author, Dr Alfonso Abizaid, associate professor at the Department of Neuroscience at Carleton University, Canada.
"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."
The team also concluded that altered postnatal leptin secretion development in mice was during the early postnatal period – a time of extreme developmental vulnerability.
“This parallels other mouse models of developmental programming such as maternal obesity food restriction and diabetes and suggests that endocrine disrupting compound-induced programming may share a common aetiology in the hypothalamic feeding circuitry,” the study stated.
Research indicates human BPA exposure is extremely common. More than 90% of people tested in population studies had detectable levels of BPA and compounds produced when it is metabolised by the body in their urine.
The concern here is foetal exposure to BPA during a critical developmental period.
A study of 244 mothers indicated that exposure to BPA before birth could affect the behaviour of girls at age 3. These girls fared worse on tests of anxiety and hyperactivity.
Maternal exposure postnatally can continue to affect the infant through transfer of BPA to the infant via breast milk .
Back in October last year, MEPs effectively voted against a large body of evidence which showed BPA to be safe at certain levels.
The MEPs chose to implement an EU-wide ban of BPA in food contact materials despite the European Food Safety Authority (EFSA) saying otherwise.
It’s most recent review, carried out in 2015, concluded there was no health risk to consumers of any age at current exposure levels.
EFSA began another evaluation of the chemical early last year with a final scientific opinion expected in 2018.
The team began by feeding pregnant mice BPA in their food exposing these animals to doses that were lower than levels deemed safe by the U.S. Food and Drug Administration.
Once the mice gave birth, the researchers gave their offspring injections of leptin at various intervals. They then examined their brain tissue and blood to assess the response to the hormone.
Other pregnant mice were either not exposed to any chemicals or were exposed to a chemical called diethylstilbestrol (DES) - a synthetic form of the female hormone oestrogen.
This was carried out so the young could be compared to those born to mice that were exposed to BPA. All the mice were fed a control diet to eliminate differences in food intake.
Newborn mice normally show a boost in leptin when they are around eight days old that programmes brain regions to respond to the feeling of fullness.
The research discovered that the mice exposed to BPA underwent this surge two days late. Mice exposed to DES did not even experience this leptin boost.
When these were given leptin over the two days, control mice that weren't subjected to either chemical experienced more weight loss than BPA- or DES-subjected mice.
The team also found mice subjected to BPA prenatally had a lower fibre density and cognitive activity in the brain region responsible for controlling energy usage.
"This study improves our understanding of how BPA can disrupt the endocrine system in a manner that raises the risk of obesity in animals," Dr Abizaid said.
"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."
Published online ahead of print: DOI: 10.1210/en.2016.1718
“Perinatal Exposure to Bisphenol-A (BPA) Delays the Postnatal Leptin Surge in Male and Female CD-1 Mice.”
Authors: Alfonso Abizaid et al