title: Stool phospholipid signature is altered by diet and tumors.
abstract: Intake of saturated fat is a risk factor for ulcerative colitis (UC) and colon cancer. Changes in the microbiota have been implicated in the development of UC and colon cancer. The host and the microbiota generate metabolites that may contribute to or reflect disease pathogenesis. We used lipid class specific quantitative mass spectrometry to assess the phospholipid (PL) profile (phosphatidylcholine [PC], phosphatidylethanolamine [PE], phosphatidylinositol [PI], phosphatidylserine [PS]) of stool from mice fed a high fat (HFD) or control diet with or without induction of colitis-associated tumors using azoxymethane and dextran sodium sulfate. The microbiota was assessed using qPCR for several bacterial groups. Colitis-associated tumors were associated with reduced bulk PI and PE levels in control diet fed mice compared to untreated mice. Significant decreases in the relative quantities of several PC species were found in colitis-associated tumor bearing mice fed either diet. Statistical analysis of the PL profile revealed distinct clustering by treatment group. Partial least squares regression analysis found that the relative quantities of the PS class profile best predicted bacterial abundance of Clostridium leptum and Prevotella groups. Abundance of selected PL species correlated with bacterial group quantities. Thus, we have described that a HFD and colitis-associated tumors are associated with changes in phospholipids and may reflect host-microbial interactions and disease states.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida, United States of America.
authors.forename: Julie M
authors.initials: JM
authors.lastname: Davies
authors.affiliation: Bascom Palmer Eye Institute, University of Miami, Miami, Florida, United States of America.
authors.forename: Hong-Uyen
authors.initials: HU
authors.lastname: Hua
authors.affiliation: Division of Gastroenterology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida, United States of America.
authors.forename: Rishu
authors.initials: R
authors.lastname: Dheer
authors.affiliation: Bascom Palmer Eye Institute, University of Miami, Miami, Florida, United States of America.
authors.forename: Mitchell
authors.initials: M
authors.lastname: Martinez
authors.affiliation: Bascom Palmer Eye Institute, University of Miami, Miami, Florida, United States of America.
authors.forename: Sanjoy K
authors.initials: SK
authors.lastname: Bhattacharya
authors.affiliation: Division of Gastroenterology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida, United States of America.
authors.forename: Maria T
authors.initials: MT
authors.lastname: Abreu
mesh_terms: D000818:Animals; D014408:Biomarkers, Tumor / Q000737:chemistry* / Q000378:metabolism; D063646:Carcinogenesis / Q000378:metabolism; D003092:Colitis / Q000209:etiology / Q000378:metabolism; D003110:Colonic Neoplasms / Q000209:etiology / Q000378:metabolism*; D059305:Diet, High-Fat / Q000009:adverse effects; D005243:Feces / Q000737:chemistry* / Q000382:microbiology; D005260:Female; D008297:Male; D008810:Mice, Inbred C57BL; D064307:Microbiota; D010743:Phospholipids / Q000737:chemistry* / Q000378:metabolism
chemical_list: D014408:Biomarkers, Tumor; D010743:Phospholipids