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Abstract

Increased maternal body mass index (BMI) is a robust risk factor for later pediatric obesity. Accumulating evidence suggests that human milk (HM) may attenuate the transfer of obesity from mother to offspring, potentially through its effects on early development of the infant microbiome. The objective of this study was to identify early differences in intestinal microbiota in a cohort of breastfeeding infants born to obese compared with normal-weight (NW) mothers. We also investigated relationships between HM hormones (leptin and insulin) and both the taxonomic and functional potential of the infant microbiome.

Study Design

Clinical data, infant stool and fasting HM samples were collected from 18 NW [prepregnancy BMI (in kg/m2) <24.0] and 12 Ob (prepregnancy BMI >30.0) mothers and their exclusively breastfed infants at 2 wk postpartum. Infant body composition at 2 wk was determined by air-displacement plethysmography. Infant gastrointestinal microbes were estimated using 16S amplicon and whole-genome sequencing. HM insulin and leptin were determined by ELISA; short-chain fatty acids (SCFAs) were measured in stool using gas chromatography. Power was set at 80%.

Key Findings

Infants born to obese mothers were exposed to 2-fold higher HM insulin and leptin concentrations and showed a significant reduction in the early pioneering bacteria Gammaproteobacteria and exhibited a trend for elevated total SCFA content. Independent of maternal prepregnancy BMI, HM insulin was positively associated with both microbial taxonomic diversity and Gammaproteobacteria and negatively associated with Lactobacillales. Metagenomic analysis revealed that HM leptin and insulin were associated with decreased bacterial proteases, which are implicated in intestinal permeability, and reduced levels of pyruvate kinase, a biomarker of pediatric gastrointestinal inflammation. The results indicate that, while maternal obesity may adversely impact the early infant intestinal microbiome, HM insulin and leptin are independently associated with beneficial microbial metabolic pathways predicted to increase intestinal barrier function and reduce intestinal inflammation.

Citation

  • Boyle KE, Patinkin ZW, Shapiro AL, Baker PR 2nd, Dabelea D, Friedman JE. Diabetes. 2016 Mar;65(3):647-59. PMID: 26631736; PMCID: PMC4764150.

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Research Details

  • Research Center: University of Colorado Anschutz Medical Campus

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