Severe riboflavin deficiency induces alterations in the hepatic proteome of starter Pekin ducks

Jing Tang, Maria A. Hegeman, Jian Hu, Ming Xie, Wenbiao Shi, Yong Jiang, Vincent de Boer, Yuming Guo, Shuisheng Hou*, Jaap Keijer

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

8 Citations (Scopus)

Abstract

Suboptimal vitamin B2 status is encountered globally. Riboflavin deficiency depresses growth and results in a fatty liver. The underlying mechanisms remain to be established and an overview of molecular alterations is lacking. We investigated hepatic proteome changes induced by riboflavin deficiency to explain its effects on growth and hepatic lipid metabolism. In all, 360 1-d-old Pekin ducks were divided into three groups of 120 birds each, with twelve replicates and ten birds per replicate. For 21 d, the ducks were fed ad libitum a control diet (CAL), a riboflavin-deficient diet (RD) or were pair-fed with the control diet to the mean daily intake of the RD group (CPF). When comparing RD with CAL and CPF, growth depression, liver enlargement, liver lipid accumulation and enhanced liver SFA (C6 : 0, C12 : 0, C16 : 0, C18 : 0) were observed. In RD, thirty-two proteins were enhanced and thirty-one diminished (>1·5-fold) compared with CAL and CPF. Selected proteins were confirmed by Western blotting. The diminished proteins are mainly involved in fatty acid β-oxidation and the mitochondrial electron transport chain (ETC), whereas the enhanced proteins are mainly involved in TAG and cholesterol biosynthesis. RD causes liver lipid accumulation and growth depression probably by impairing fatty acid β-oxidation and ETC. These findings contribute to our understanding of the mechanisms of liver lipid metabolic disorders due to RD.

Original languageEnglish
Pages (from-to)641-650
JournalThe British journal of nutrition
Volume118
Issue number9
DOIs
Publication statusPublished - 14 Nov 2017

Keywords

  • β-Oxidation
  • ACAD9 acyl-CoA dehydrogenase family member 9
  • ACADM medium-chain specific acyl-CoA dehydrogenase
  • ACADS short-chain specific acyl-CoA dehydrogenase
  • ACAT2 acetyl-CoA acetyltransferase
  • APOB apo B-100 CAL fed ad libitum a control diet
  • CPF
  • DLD dihydrolipoyl dehydrogenase
  • ETC electron transport chain
  • ETFDH electron transfer flavoprotein-ubiquinone oxidoreductase
  • FXN frataxin
  • HMGCS1 hydroxymethylglutaryl-CoA synthase
  • MDH1 malate dehydrogenase
  • MTTP microsomal TAG transfer protein
  • NDUFA8 NADH dehydrogenase (ubiquinone) 1α subcomplex subunit 8
  • NDUFS1 NADH-ubiquinone oxidoreductase 75 kDa subunit
  • pair-fed with the control diet to the mean daily intake of the riboflavin-deficient group
  • RD riboflavin-deficient diet
  • SCP2 non-specific lipid-transfer protein
  • TC total cholesterol
  • TCA tricarboxylic acid
  • Electron transport chain
  • Lipid metabolism
  • Liver proteomics
  • Riboflavin deficiency

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