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Maternal obesity alters gut microbial ecology in offspring of NOD mice
Author(s) -
Zhu Meijun,
Kang Yifei,
Du Min
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.601.4
Subject(s) - offspring , lachnospiraceae , biology , bacteroidetes , firmicutes , endocrinology , medicine , bacteroidaceae , gut flora , pregnancy , genetics , immunology , bacteria , 16s ribosomal rna
Background Gut microbiota (GM) are increasingly recognized as a significant factor in the pathogenesis of T1D. High Bacteroidetes / Firmicutes (B/F) is associated with the development of T1D. Previously we reported that maternal obesity (MO) increases the incidence of T1D in the offspring of nonobese diabetic (NOD) mice, and the current study investigated the possible link of GM to the exaggerated insulitis in offspring due to MO. Methods: 4‐wk‐old female NOD mice were fed either a control or a high fat diet for 8 weeks before mating. Mice were maintained in their respective diets during pregnancy and lactation. All offspring were fed the control diet to 16‐wk‐old. Results Pyrosequencing examination revealed that GM of offspring born to obese mothers was distinct from those of control mothers. At phylum level, MO increased Bacteroidetes , Defferibacteres and Proteobacteria , while decreased Firmicutes in offspring GM, resulting in increased B/F ratio in GM of obese offspring. Family level analysis indicated that GM of offspring from obese mothers had increased levels of Deferribacteraceae , Bacteroidaceae, Desulfovibrionaceae, Helicobacteraceaev, and Porphyromonadaceae . Reciprocally, the abundance of Rikenellaceae and Lachnospiraceae‐Ruminococcaceae were decreased in offspring from obese mothers. The analysis at the genus level revealed that Bacteriodes, Barnesiella, Desulfovibrio and Mucispirillum were more abundance, while Alistipes, Clostridium XIVa, Dorea and Osillibacter were less abundance in offspring of obese mothers. Conclusion MO resulted in a dysbiosis in offspring, suggesting a GM‐mediated mechanism on diabetogenesis by MO (NIH R15HD073864).