Maternal gut microbiota in pregnancy influences offspring metabolic phenotype in mice

TLDR

Maternal gut microbiota influence offspring metabolic health, as obesity is linked to type 2 diabetes and cardiovascular disease, and short‑chain fatty acids from the microbiota suppress insulin signaling and reduce fat deposition. Kimura et al. examined whether maternal microbiota protect offspring from obesity by studying germ‑free mice on high‑fat diets. They found that maternal SCFAs cross the placenta, with propionate acting through GPR43 to regulate insulin and through GPR41 to influence sympathetic development; a high‑fiber diet increased propionate and protected offspring, whereas antibiotic treatment produced obesity‑prone progeny.

Abstract

Mouse mothers transfer metabolic mode Obesity and metabolic diseases tend to go together, and humans who become obese are also prone to type 2 diabetes and cardiovascular problems. Starting with the observation that offspring of germ-free mice tended to become obese on high-fat diets, Kimura et al. investigated how the presence of the microbiota might be protective in mice (see the Perspective by Ferguson). short-chain fatty acids (SCFAs) from the microbiota are known to suppress insulin signaling and reduce fat deposition in adipocytes. Further experiments showed that SCFAs in the bloodstream were able to pass from a non–germ-free mother's gut microbiota across the placenta and into the developing embryos. The authors found that in the embryos, the SCFA propionate mediates not only insulin levels through GPR43 signaling but also sympathetic nervous system development through GPR41 signaling. A high-fiber diet promoted propionate production from the maternal microbiota, and maternal antibiotic treatment resulted in obese-prone offspring. Science , this issue p. eaaw8429 ; see also p. 978