Associations between maternal obesity and offspring gut microbiome in the first year of life

Pediatr Obes. 2022 Sep;17(9):e12921. doi: 10.1111/ijpo.12921. Epub 2022 Apr 27.

Abstract

Background: Maternal obesity is an important determinant of offspring obesity risk, which may be mediated via changes in the infant microbiome.

Objectives: We examined infant faecal microbiome, short-chain fatty acids (SCFA), and maternal human milk oligosaccharides (HMO) in mothers with overweight/obese body mass index (BMI) (OW) compared with normal weight (NW) (Clinicaltrials.gov NCT01131117).

Methods: Infant stool samples at 1, 6, and 12 months were analysed by 16S rRNA sequencing. Maternal (BODPOD) and infant (quantitative nuclear magnetic resonance [QMR]) adiposity were measured. HMOs at 2 months postpartum and faecal SCFAs at 1 month were also assessed. Statistical analyses included multivariable and mixed linear models for assessment of microbiome diversity, composition, and associations of taxonomic abundance with metabolic and anthropometric variables.

Results: At 1 month, offspring of women with obesity had lower abundance of SCFA-producing bacteria (including Ruminococcus and Turicibacter) and lower faecal butyric acid levels. Lachnospiraceae abundance was lower in OW group at 6 months, and infant fat mass was negatively associated with the levels of Sutterella. Gradient boosting machine models indicated that higher α-diversity and specific microbial taxa at 1 month predicted elevated adiposity at 12 months with overall accuracy of 76.5%. Associations between maternal HMO concentrations and infant bacterial taxa differed between NW and OW groups.

Conclusions: Elevated maternal BMI is associated with relative depletion of butyrate-producing microbes and faecal butyrate in the early infant faecal microbiome. Overall microbial richness may aid in prediction of elevated adiposity in later infancy.

Keywords: adiposity; human milk oligosaccharides; infant; maternal obesity; microbiome.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, N.I.H., Extramural

MeSH terms

  • Bacteria / genetics
  • Butyrates
  • Female
  • Gastrointestinal Microbiome* / genetics
  • Humans
  • Infant
  • Milk, Human / metabolism
  • Obesity / epidemiology
  • Obesity / metabolism
  • Oligosaccharides
  • Pregnancy
  • Pregnancy in Obesity*
  • RNA, Ribosomal, 16S

Substances

  • Butyrates
  • Oligosaccharides
  • RNA, Ribosomal, 16S

Associated data

  • ClinicalTrials.gov/NCT01131117