Western diet strongly influences gut microbiomes in nursing rat dams but translates modest long‐term consequences to offspring modulated by leptin supplementation during suckling

Abstract Early life conditions may influence the gut microbiome and contribute to health status in adulthood. We examined the impact of maternal obesity and/or obesogenic diet on the gut microbiome of mothers (at weaning) and their adult offspring, along with the effects of leptin supplementation during suckling. Three groups of rats were studied: control (C) dams, fed with standard diet (SD); western diet (WD) dams, fed with WD (a high‐fat, high‐sucrose diet) before gestation and during gestation and lactation; and reversion (REV) dams, fed as WD‐dams but with SD during lactation. Offspring were supplemented throughout suckling with leptin/vehicle and weaned on an SD. WD‐dams showed lower microbial diversity and an altered microbiome compared to C‐ and REV‐dams, widely normalized by diet improvement during lactation. WD‐ and REV‐offspring (males) displayed lower microbiome diversity and greater dominance compared to C‐offspring. Taxonomic group differences (Proteobacteria phylum and Bacteroides, Parasutterella, and Phocea genera) were observed in WD‐ and REV‐offspring. WD‐offspring, but not REV‐offspring, had a greater abundance of the phylum Firmicutes and Lachnospiraceae family and a lower abundance of the family Tannerellaceae compared to C‐offspring. Leptin supplementation led to decreased abundance of the phylum Actinobacteria (family Eggerthellaceae and genera Enterorhabdus and Adlercreutzia (females)), and the genera Lachnospiraceae UCG‐008 group, Roseburia and Limosilactobacillus, and increased abundance of the genus Dellaglioa, compared to vehicle‐treated groups. Therefore, maternal consumption of an obesogenic diet during the perinatal period results in microbiome changes in dams, alleviated by dietary improvement during lactation. Maternal conditions and leptin supplementation during suckling modestly influenced the microbiome in adulthood, which might partially contribute to the adverse/beneficial effects, respectively, of these conditions on programmed metabolic health.