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Composition of Dietary Fat Source Shapes Gut Microbiota Architecture and Alters Host Inflammatory Mediators in Mouse Adipose Tissue
Author(s) -
Huang Edmond,
Leone Vanessa,
Devkota Suzanne,
Wang Yunwei,
Brady Matthew,
Donovan Sharon,
Chang Eugene
Publication year - 2013
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.27.1_supplement.361.3
Subject(s) - adipose tissue , gut flora , inflammation , resistin , obesity , biology , medicine , endocrinology , polyunsaturated fatty acid , immunology , insulin resistance , adiponectin , biochemistry , fatty acid
High‐fat diet consumption has a significant impact on the development of obesity and inflammation. Studies have shown that dietary factors alter gut microbiota resulting in metabolic and immunologic effects within the host through adipose tissue. The objective of this study is to address how consumption of specific high saturated (SFA) and polyunsaturated (PUFA) fat shapes the intestinal microbiota and how these changes affect adipose tissue‐mediated inflammation. Adult male C57Bl/6 mice were fed SFA and PUFA diets for four weeks. Body mass and food consumption data were collected weekly. Bacterial DNA from stool samples was extracted and analyzed by T‐RFLP and HiSeq methods. Adipose depots were excised and analyzed for lipogenic and inflammatory gene expression via qRT‐PCR. Mice fed high‐fat diets showed increased caloric consumption and weight gain compared to low‐fat fed mice. High‐fat diets also resulted in a dramatic shift in gut microbiota, stratifying based on the specific source of dietary fat. These changes led to significantly altered expression of inflammatory markers (MCP‐1, CD192, resistin, APN) in adipose depots. Collectively, our findings show that gut microbiota resulting from dietary modulation of fat source can influence inflammatory outcome and should be considered a potential therapeutic target to alleviate obesity‐induced inflammation. Grant Funding Source : T32 DK07074