Mutation of the lbp-5 gene alters metabolic output in Caenorhabditis elegans

Mo Xu, Eun Young Choi, Young-Ki Paik

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Intracellular lipid-binding proteins (LBPs) impact fatty acid homeostasis in various ways, including fatty acid transport into mitochondria. However, the physiological consequences caused by mutations in genes encoding LBPs remain largely uncharacterized. Here, we explore the metabolic consequences of lbp-5 gene deficiency in terms of energy homeostasis in Caenorhabditis elegans. In addition to increased fat storage, which has previously been reported, deletion of lbp-5 attenuated mitochondrial membrane potential and increased reactive oxygen species levels. Biochemical measurement coupled to proteomic analysis of the lbp-5(tm1618) mutant revealed highly increased rates of glycolysis in this mutant. These differential expression profile data support a novel metabolic adaptation of C. elegans, in which glycolysis is activated to compensate for the energy shortage due to the insufficient mitochondrial βl-oxidation of fatty acids in lbp-5 mutant worms. This report marks the first demonstration of a unique metabolic adaptation that is a consequence of LBP-5 deficiency in C. elegans.

Original languageEnglish
Pages (from-to)15-20
Number of pages6
JournalBMB reports
Volume47
Issue number1
DOIs
Publication statusPublished - 2014 Jan 1

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Caenorhabditis elegans
Carrier Proteins
Fatty Acids
Genes
Glycolysis
Lipids
Mutation
Homeostasis
Protein Deficiency
Fatty Acid-Binding Proteins
Mitochondria
Gene encoding
Mitochondrial Membrane Potential
Proteomics
Reactive Oxygen Species
Demonstrations
Fats
Membranes
Oxidation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

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Mutation of the lbp-5 gene alters metabolic output in Caenorhabditis elegans. / Xu, Mo; Choi, Eun Young; Paik, Young-Ki.

In: BMB reports, Vol. 47, No. 1, 01.01.2014, p. 15-20.

Research output: Contribution to journalArticle

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