What is already known on this topic
Obesity is often associated with type 2 diabetes and cardiovascular problems. Several studies have shown that a mother’s gut microbiota influences the risk of cardiometabolic disease in offspring, but the mechanisms underlying this connection are unclear.
What this research adds
Using mouse models, researchers found that a mother’s gut microbes confer resistance to obesity to their offspring. Microbiota-derived short chain fatty acids influenced the differentiation of the offspring’s neural, intestinal, and pancreatic cells through signals sent from specific protein receptors on the surface of fat cells. This process helped to prevent metabolic syndrome in newborn mice, whereas offspring from mothers that lacked microbes altogether were highly susceptible to conditions such as obesity and glucose intolerance.
The findings suggest that targeting the maternal microbiota – through, for example, dietary interventions – could help to protect offspring from future metabolic disease.
Obesity, diabetes, and cardiovascular problems often result from a combination of inherited factors and personal diet and exercise choices. Now, a study in mice suggests that a mother’s gut microbes shape the metabolism of offspring, conferring resistance to obesity.
The findings, published in Science, may lead to new strategies that target the maternal microbiota to protect offspring from future metabolic disease.
Several studies have shown that a mother’s gut microbiota influences the risk of cardiometabolic disease in offspring, but the mechanisms underlying this connection are unclear.
To learn more about the impact of a mother’s gut microbiota on the health of her baby, a team of researchers led by Ikuo Kimura and Junki Miyamoto at Tokyo University of Agriculture and Technology studied pregnant mice that lived under either normal or germ-free conditions.
Starting from the observation that microbiota-derived short-chain fatty acids (SCFAs), including propionate, acetate, and butyrate, are linked to obesity and insulin sensitivity, the researchers tested the role of microbial SCFA production on fetal development.
Mice whose mothers lacked microbes altogether were highly susceptible to diet-induced obesity later in life and showed signs of glucose intolerance and insulin resistance. Mice born to conventionally raised mothers did not experience any of these effects.
The researchers observed no differences in the gut microbiota composition of the offspring of mothers that lacked microbes compared to that of mothers that did have microbes. But the team found differences in the amounts of circulating SCFAs such as acetate, propionate, and butyrate in both the mothers and offspring when comparing germ-free and conventionally raised mice.
The researchers found that SCFAs produced by the pregnant mother’s gut microbes influenced the differentiation of the offspring’s neural, intestinal and pancreatic cells through signals sent from specific protein receptors on the surface of fat cells. This process helped to balance energy levels in offspring. The offspring of mice lacking those protein receptors on the surface of fat cells were more susceptible to obesity and metabolic conditions such as glucose intolerance.
Giving pregnant mice the SCFA propionate protected offspring against future disease, the researchers found. “However, whether propionate supplementation had any effects on the mother was not assessed,” says Jane Ferguson, a researcher at Vanderbilt University Medical Center in Nashville, Tennessee, who was not involved in the study.
More research is needed to find out if SCFAs work the same way in people, and if so, to find out if prescribing supplements such as propionate to pregnant women could help reduce the risk of metabolic syndrome in babies, Ferguson says.