Fig. 1

HIP leads to gut microbiota alterations and metabolic deficits in mouse offspring. a Hyperglycaemia in pregnancy (HIP) model and experimental scheme of the mice. b Body weight and c blood glucose levels and areas under the curve (AUCs) during the oral glucose tolerance test (OGTT) of the mHF group and the mNC group. d Body weight, e blood glucose levels and AUCs during the OGTT, f serum insulin levels by ELISA and AUCs during the OGTT and g changes in blood glucose levels (% of initial) and AUCs during the insulin tolerance test (ITT) of offspring of the mHF and mNC groups (HF and NC groups, respectively). h The amount of insulin secretion upon stimulation with 3.3 mmol/L (low) and 16.7 mmol/L (high) glucose and the glucose stimulation index (GSI) of islets isolated from pancreatic tissues of the offspring of the mHF and mNC groups. i Pdx-1 and MafA mRNA expression levels by qPCR in pancreatic tissues of offspring of the mHF and mNC groups. Data are presented as the mean ± SD; *P<0.05, **P<0.01, ***P<0.001. j Principal coordinate analysis (PCoA) of the maternal mice and their offspring on the first two principal coordinates was performed based on the Jaccard distance. Comparisons were performed using the Kruskal–Wallis test for significant differences, *P<0.05, **P<0.01, ***P<0.001. k Identification of major amplicon sequence variants (ASVs) contributing to the differences in the gut microbiota of the offspring groups using Linear discriminant analysis Effect Size (LEfSe). mHF (n=7): maternal group with high-fat diet; mNC (n=8): maternal group with normal control diet; HF (n=10): offspring delivered by mHF group; NC (n=10): offspring delivered by the mNC group