title: Intestinal and systemic inflammatory responses are positively associated with sulfidogenic bacteria abundance in high-fat-fed male C57BL/6J mice.
abstract: Recent studies have highlighted the relation between high-fat (HF) diets, the gut microbiota, and inflammation. However, the role of sulfidogenic bacteria in mediating these effects has been explored only recently. Therefore, we tested the hypothesis that an HF diet rich in saturated fat stimulates sulfidogenic bacteria and that these increases correlate with intestinal and systemic inflammatory responses. Forty C57BL/6J male mice were fed a low-fat (LF; 10% of energy) or an HF lard-based (60% of energy) diet for 6 or 20 wk. Mucosa samples were collected from the ileum, cecum, and colon and used for measuring 16S ribosomal RNA and functional genes of sulfidogenic bacteria. Matching intestinal samples and visceral and subcutaneous white adipose tissue (WAT) depots were used to measure mRNA abundance for inflammatory genes. Mice fed the HF diet had greater (P < 0.05) abundance of 3 types of sulfidogenic bacteria, primarily in colonic mucosa, compared with LF-fed mice at week 20. Although HF feeding did not increase intestinal inflammation at week 6, ileal markers of macrophage infiltration and inflammation were upregulated (P < 0.05) 1- to 6-fold at week 20. HF feeding impaired the localization of the tight junction protein zonula occludens 1 at the apical area of the ileal epithelium at weeks 6 and 20. Mice fed the HF diet had 1- to 100-fold greater (P < 0.05) mRNA levels of markers of macrophage infiltration in visceral and subcutaneous WAT at week 20, but not at week 6, compared with LF-fed mice. These results provide evidence that chronic, but not acute, consumption of an HF lard-based diet may be linked with pathways of microbial metabolism that potentially contribute to chronic intestinal and systemic inflammation. Such linkage provides further support for reducing consumption of saturated fats.
authors.affiliation: Department of Nutrition, University of North Carolina, Greensboro, NC.
authors.forename: Wan
authors.initials: W
authors.lastname: Shen
authors.affiliation: Institute of Genomic Biology, University of Illinois, Urbana-Champaign, IL.
authors.forename: Patricia G
authors.initials: PG
authors.lastname: Wolf
authors.affiliation: Department of Food Science, University of Arkansas, Fayetteville, AR; and.
authors.forename: Franck
authors.initials: F
authors.lastname: Carbonero
authors.affiliation: Center for Translational Biomedical Research, University of North Carolina-North Carolina Research Campus, Kannapolis, NC.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhong
authors.affiliation: Department of Nutrition, University of North Carolina, Greensboro, NC.
authors.forename: Tanya
authors.initials: T
authors.lastname: Reid
authors.affiliation: Institute of Genomic Biology, University of Illinois, Urbana-Champaign, IL.
authors.forename: H Rex
authors.initials: HR
authors.lastname: Gaskins
authors.affiliation: Department of Nutrition, University of North Carolina, Greensboro, NC mkmcinto@uncg.edu.
authors.forename: Michael K
authors.initials: MK
authors.lastname: McIntosh
mesh_terms: D000818:Animals; D001419:Bacteria / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D059305:Diet, High-Fat; D004041:Dietary Fats / Q000008:administration & dosage*; D007249:Inflammation / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D050151:Subcutaneous Fat
chemical_list: D015415:Biomarkers; D004041:Dietary Fats; D012336:RNA, Ribosomal, 16S