Host remodeling of the gut microbiome and metabolic changes during pregnancy

Omry Koren, Julia K. Goodrich, Tyler C. Cullender, Aymé Spor, Kirsi Laitinen, Helene Kling Bäckhed, Antonio Gonzalez, Jeffrey J. Werner, Largus T. Angenent, Rob Knight, Fredrik Bäckhed, Erika Isolauri, Seppo Salminen, Ruth E. Ley

Research output: Contribution to journalArticlepeer-review

1632 Scopus citations

Abstract

Many of the immune and metabolic changes occurring during normal pregnancy also describe metabolic syndrome. Gut microbiota can cause symptoms of metabolic syndrome in nonpregnant hosts. Here, to explore their role in pregnancy, we characterized fecal bacteria of 91 pregnant women of varying prepregnancy BMIs and gestational diabetes status and their infants. Similarities between infant-mother microbiotas increased with children's age, and the infant microbiota was unaffected by mother's health status. Gut microbiota changed dramatically from first (T1) to third (T3) trimesters, with vast expansion of diversity between mothers, an overall increase in Proteobacteria and Actinobacteria, and reduced richness. T3 stool showed strongest signs of inflammation and energy loss; however, microbiome gene repertoires were constant between trimesters. When transferred to germ-free mice, T3 microbiota induced greater adiposity and insulin insensitivity compared to T1. Our findings indicate that host-microbial interactions that impact host metabolism can occur and may be beneficial in pregnancy.

Original languageEnglish
Pages (from-to)470-480
Number of pages11
JournalCell
Volume150
Issue number3
DOIs
StatePublished - 3 Aug 2012
Externally publishedYes

Bibliographical note

Funding Information:
We thank Mary-Claire King, Andrew Clark, and Andrew Gewirtz for their contributions to the manuscript, and we thank Daniel McDonlad and Nick Scalfone for technical assistance. This research was supported by The Hartwell Foundation, the NIH Human Microbiome Project DACC, the David and Lucile Packard Foundation, the Arnold and Mabel Beckman Foundation, the Cornell Center for Comparative Population Genomics, the Ragnar Söderberg Foundation, the Päivikki and Sakari Sohlberg Foundation, and the Academy of Finland.

Funding

We thank Mary-Claire King, Andrew Clark, and Andrew Gewirtz for their contributions to the manuscript, and we thank Daniel McDonlad and Nick Scalfone for technical assistance. This research was supported by The Hartwell Foundation, the NIH Human Microbiome Project DACC, the David and Lucile Packard Foundation, the Arnold and Mabel Beckman Foundation, the Cornell Center for Comparative Population Genomics, the Ragnar Söderberg Foundation, the Päivikki and Sakari Sohlberg Foundation, and the Academy of Finland.

FundersFunder number
Cornell Center for Comparative
Ragnar Söderberg Foundation
National Institutes of Health
David and Lucile Packard Foundation
NIH Office of the DirectorDP2OD007444
National Institute of Diabetes and Digestive and Kidney DiseasesR01DK093595
Arnold and Mabel Beckman Foundation
Hartwell Foundation
Academy of Finland
Päivikki ja Sakari Sohlbergin Säätiö

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