High-fat maternal diet during pregnancy persistently alters the offspring microbiome in a primate model.
The intestinal microbiome is a unique ecosystem and an essential mediator of metabolism and obesity in mammals. However, studies investigating the impact of the diet on the establishment of the gut microbiome early in life are generally lacking, and most notably so in primate models. Here we report that a high-fat maternal or postnatal diet, but not obesity per se, structures the offspring's intestinal microbiome in Macaca fuscata (Japanese macaque). The resultant microbial dysbiosis is only partially corrected by a low-fat, control diet after weaning. Unexpectedly, early exposure to a high-fat diet diminished the abundance of non-pathogenic Campylobacter in the juvenile gut, suggesting a potential role for dietary fat in shaping commensal microbial communities in primates. Our data challenge the concept of an obesity-causing gut microbiome and rather provide evidence for a contribution of the maternal diet in establishing the microbiota, which in turn affects intestinal maintenance of metabolic health.
1] Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA [2] Department of Molecular and Human Genetics, Bioinformatics Research Lab at Baylor College of Medicine, Houston, Texas 77030, USA [3].
Jun
J
Ma
1] Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA [2].
Amanda L
AL
Prince
1] Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA [2] Department of Molecular and Cell Biology at Baylor College of Medicine, Houston, Texas 77030, USA [3].
David
D
Bader
Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA.
Min
M
Hu
Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA.
Radhika
R
Ganu
Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97239, USA.
Karalee
K
Baquero
Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97239, USA.
Peter
P
Blundell
1] Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA [2] Department of Molecular and Human Genetics, Bioinformatics Research Lab at Baylor College of Medicine, Houston, Texas 77030, USA.
R
R
Alan Harris
Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97239, USA.
Antonio E
AE
Frias
Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97239, USA.
Kevin L
KL
Grove
1] Departments of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine at Baylor College of Medicine and Texas Children's Hospital, Houston, Texas 77030, USA [2] Department of Molecular and Human Genetics, Bioinformatics Research Lab at Baylor College of Medicine, Houston, Texas 77030, USA [3] Department of Molecular and Cell Biology at Baylor College of Medicine, Houston, Texas 77030, USA.
Kjersti M
KM
Aagaard
D000818:Animals; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat / Q000009:adverse effects*; D064806:Dysbiosis / Q000209:etiology* / Q000382:microbiology; D005260:Female; D007422:Intestines / Q000382:microbiology*; D008251:Macaca; D064307:Microbiota; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology* / Q000382:microbiology; D014886:Weaning