The study used rats to test how consumption of a diet containing excessive fats during pregnancy and lactation affects neural activity and weight management in later life of offspring.
Findings published in the Journal of Physiology suggest maternal and perinatal diet has ‘significant effects’ on brain regions that control feeding and satiety, say the US-based authors behind the study.
"It's time that we start to take seriously the idea that obesity is, in part, a brain disease," commented Dr Kirsteen Browning from Penn State College of Medicine – the lead investigator of the research.
"We looked at the circuits that relay information from the stomach and the small intestine to the brain and back to the stomach telling it how to work," she explained, noting that these normal reflex mechanisms, which help limit the amount of food we eat, can malfunction and become less sensitive in obesity.
"We found that parts of these reflexes were actually compromised even before we saw obesity,” said Browning. "Rats on the high-fat diet looked exactly the same as the control group rats in terms of weight, but their feeding reflexes were already beginning to be compromised."
In the new study, the Penn State team fed one group of rats a high-fat diet (HFD) containing 60% calories from fat during pregnancy and lactation – known as the perinatal period - while another group were fed a control diet containing around 13.5% of calories from fat. Offspring were then fed the same diet after weaning for 21 days. When the rats reached adolescence, at aproximately 35–42 days of age, the team then measured neural activity involved in energy balance and appetite regulation.
“The present study was designed to test the hypothesis that exposure to a HFD during the perinatal period alters the electrophysiological, pharmacological and morphological properties of vagal efferent motoneurones innervating the stomach,” wrote the team.
They found that consumption of a high-fat diet decreases the excitability of certain nerves involved in appetite control and satiety (gastric-projecting dorsal motor nucleus neurones) and dysregulates neurotransmitter release.
Significantly, the team noted that these alterations occurred prior to the development of obesity.
“These findings represent the first direct evidence that exposure to a HFD modulates the processing of central vagal neurocircuits even in the absence of obesity,” said Browning and her collegaues.
Exactly how maternal diet influences these functions is still unknown, the team added.
Browning now plans to do more research to determine the precise perinatal timeframe within which feeding neurocircuits are vulnerable to unhealthy alterations, and perhaps most importantly whether these changes can be reversed once set into motion.
She also wants to test whether the fat content or the caloric load of the rats' diet induced the changes.
Source: Journal of Physiology
Volume 593, Issue 1, Pages 285–303, doi: 10.1113/jphysiol.2014.282806
“Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity”
Authors: Ruchi Bhagat, et al