Background: Overweight or obese pregnant women have increased risk of adverse outcomes, some of which have been linked to alterations in the gut microbiome and dysbiosis. The short-chain fatty acid butyrate is produced by the gut microbiota and widely viewed as a biomarker of healthy gut function because of its effects on gut homeostasis, inflammation, epigenetic regulation and pancreatic beta cell function.
Aim: This study compares the butyrate-producing capacity of intestinal bacteria and gut microbial profiles between 88 overweight (BMI 25-29.9 kg/m2), 97 obese (BMI 30-39.9 kg/m2) and 30 morbidly obese (>40 kg/m2) women at 16 weeks gestation from the SPRING cohort1.
Methods: Quantification of the main bacterial butyrate-synthesis genes, butyryl-CoA:acetate CoA-transferase (BCoATscr aka BUT) and butyrate-kinase (BUK) were assessed by quantitative PCR.Fecal microbiota profiles (n=108) were assessed by 16S rRNA sequencing and the relative abundances of butyrate producers from Clostridium clusters IV and XIVa were compared.
Results: BUT and BUK copy numbers were variable among women (BUT range 1.4 x 105 - 2.3 x 108 copies/15 ng DNA, BUKrange 0 - 7.8 x 106 copies/15 ng DNA). Copy numbers of both BUT and BUK were negatively correlated with maternal BMI (BUT: Spearman’s rho -0.139, p=0.04, BUK: Spearman’s rho -0.141, p=0.03). 31 women who developed gestational diabetes mellitus (GDM) at 28 weeks gestation displayed lower BUTcopy numbers compared to non-GDM (p=0.012) but no difference in BUK copy numbers (p=0.156) at 16 weeks gestation. Relative abundances of the known butyrate producers from Clostridium clusters IV and XIVa were positively associated with BUT copy numbers (Spearman’s rho 0.221, p=0.022).
Conclusion: Pregnant women with a higher BMI have lower butyrate-producing capacity in their gut microbiome, which may influence their inflammatory and metabolic health: women who later developed GDM had lower copy numbers of the main butyrate producing gene BUT.