Effects of dietary different doses of copper and high fructose feeding on rat fecal metabolome

Xiaoli Wei, Ming Song, Xinmin Yin, Dale A. Schuschke, Imhoi Koo, Craig J. McClain, Xiang Zhang

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The gut microbiota plays a critical role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Increased fructose consumption and inadequate copper intake are two critical risk factors in the development of NAFLD. To gain insight into the role of gut microbiota, fecal metabolites, obtained from rats exposed to different dietary levels of copper with and without high fructose intake for 4 weeks, were analyzed by comprehensive two-dimensional gas chromatography time-of-flight mass spectrometry (GC × GC-TOF MS). In parallel, liver tissues were assessed by histology and triglyceride assay. Our data showed that high fructose feeding led to obvious hepatic steatosis in both marginal copper deficient rats and copper supplementation rats. Among the 38 metabolites detected with significant abundance alteration between groups, short chain fatty acids were markedly decreased with excessive fructose intake irrespective of copper levels. C15:0 and C17:0 long chain fatty acids, produced only by bacteria, were increased by either high copper level or high fructose intake. In addition, increased fecal urea and malic acid paralleled the increased hepatic fat accumulation. Collectively, GC × GC-TOF MS analysis of rat fecal samples revealed distinct fecal metabolome profiles associated with the dietary high fructose and copper level, with some metabolites possibly serving as potential noninvasive biomarkers of fructose induced-NAFLD.

Original languageEnglish (US)
Pages (from-to)4050-4058
Number of pages9
JournalJournal of Proteome Research
Volume14
Issue number9
DOIs
StatePublished - Sep 4 2015

Fingerprint

Metabolome
Fructose
Rats
Copper
Liver
Metabolites
Histology
Volatile Fatty Acids
Biomarkers
Gas chromatography
Gas Chromatography
Mass spectrometry
Urea
Assays
Mass Spectrometry
Bacteria
Triglycerides
Fatty Acids
Fats
Tissue

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Chemistry(all)

Cite this

Wei, Xiaoli ; Song, Ming ; Yin, Xinmin ; Schuschke, Dale A. ; Koo, Imhoi ; McClain, Craig J. ; Zhang, Xiang. / Effects of dietary different doses of copper and high fructose feeding on rat fecal metabolome. In: Journal of Proteome Research. 2015 ; Vol. 14, No. 9. pp. 4050-4058.
@article{3647e4d0b6c44757a9446dd95665b932,
title = "Effects of dietary different doses of copper and high fructose feeding on rat fecal metabolome",
abstract = "The gut microbiota plays a critical role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Increased fructose consumption and inadequate copper intake are two critical risk factors in the development of NAFLD. To gain insight into the role of gut microbiota, fecal metabolites, obtained from rats exposed to different dietary levels of copper with and without high fructose intake for 4 weeks, were analyzed by comprehensive two-dimensional gas chromatography time-of-flight mass spectrometry (GC × GC-TOF MS). In parallel, liver tissues were assessed by histology and triglyceride assay. Our data showed that high fructose feeding led to obvious hepatic steatosis in both marginal copper deficient rats and copper supplementation rats. Among the 38 metabolites detected with significant abundance alteration between groups, short chain fatty acids were markedly decreased with excessive fructose intake irrespective of copper levels. C15:0 and C17:0 long chain fatty acids, produced only by bacteria, were increased by either high copper level or high fructose intake. In addition, increased fecal urea and malic acid paralleled the increased hepatic fat accumulation. Collectively, GC × GC-TOF MS analysis of rat fecal samples revealed distinct fecal metabolome profiles associated with the dietary high fructose and copper level, with some metabolites possibly serving as potential noninvasive biomarkers of fructose induced-NAFLD.",
author = "Xiaoli Wei and Ming Song and Xinmin Yin and Schuschke, {Dale A.} and Imhoi Koo and McClain, {Craig J.} and Xiang Zhang",
year = "2015",
month = "9",
day = "4",
doi = "10.1021/acs.jproteome.5b00596",
language = "English (US)",
volume = "14",
pages = "4050--4058",
journal = "Journal of Proteome Research",
issn = "1535-3893",
publisher = "American Chemical Society",
number = "9",

}

Effects of dietary different doses of copper and high fructose feeding on rat fecal metabolome. / Wei, Xiaoli; Song, Ming; Yin, Xinmin; Schuschke, Dale A.; Koo, Imhoi; McClain, Craig J.; Zhang, Xiang.

In: Journal of Proteome Research, Vol. 14, No. 9, 04.09.2015, p. 4050-4058.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of dietary different doses of copper and high fructose feeding on rat fecal metabolome

AU - Wei, Xiaoli

AU - Song, Ming

AU - Yin, Xinmin

AU - Schuschke, Dale A.

AU - Koo, Imhoi

AU - McClain, Craig J.

AU - Zhang, Xiang

PY - 2015/9/4

Y1 - 2015/9/4

N2 - The gut microbiota plays a critical role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Increased fructose consumption and inadequate copper intake are two critical risk factors in the development of NAFLD. To gain insight into the role of gut microbiota, fecal metabolites, obtained from rats exposed to different dietary levels of copper with and without high fructose intake for 4 weeks, were analyzed by comprehensive two-dimensional gas chromatography time-of-flight mass spectrometry (GC × GC-TOF MS). In parallel, liver tissues were assessed by histology and triglyceride assay. Our data showed that high fructose feeding led to obvious hepatic steatosis in both marginal copper deficient rats and copper supplementation rats. Among the 38 metabolites detected with significant abundance alteration between groups, short chain fatty acids were markedly decreased with excessive fructose intake irrespective of copper levels. C15:0 and C17:0 long chain fatty acids, produced only by bacteria, were increased by either high copper level or high fructose intake. In addition, increased fecal urea and malic acid paralleled the increased hepatic fat accumulation. Collectively, GC × GC-TOF MS analysis of rat fecal samples revealed distinct fecal metabolome profiles associated with the dietary high fructose and copper level, with some metabolites possibly serving as potential noninvasive biomarkers of fructose induced-NAFLD.

AB - The gut microbiota plays a critical role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Increased fructose consumption and inadequate copper intake are two critical risk factors in the development of NAFLD. To gain insight into the role of gut microbiota, fecal metabolites, obtained from rats exposed to different dietary levels of copper with and without high fructose intake for 4 weeks, were analyzed by comprehensive two-dimensional gas chromatography time-of-flight mass spectrometry (GC × GC-TOF MS). In parallel, liver tissues were assessed by histology and triglyceride assay. Our data showed that high fructose feeding led to obvious hepatic steatosis in both marginal copper deficient rats and copper supplementation rats. Among the 38 metabolites detected with significant abundance alteration between groups, short chain fatty acids were markedly decreased with excessive fructose intake irrespective of copper levels. C15:0 and C17:0 long chain fatty acids, produced only by bacteria, were increased by either high copper level or high fructose intake. In addition, increased fecal urea and malic acid paralleled the increased hepatic fat accumulation. Collectively, GC × GC-TOF MS analysis of rat fecal samples revealed distinct fecal metabolome profiles associated with the dietary high fructose and copper level, with some metabolites possibly serving as potential noninvasive biomarkers of fructose induced-NAFLD.

UR - http://www.scopus.com/inward/record.url?scp=84941127258&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84941127258&partnerID=8YFLogxK

U2 - 10.1021/acs.jproteome.5b00596

DO - 10.1021/acs.jproteome.5b00596

M3 - Article

C2 - 26216400

AN - SCOPUS:84941127258

VL - 14

SP - 4050

EP - 4058

JO - Journal of Proteome Research

JF - Journal of Proteome Research

SN - 1535-3893

IS - 9

ER -