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

BMB Rep. 2014 Jan;47(1):15-20. doi: 10.5483/bmbrep.2014.47.1.086.


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 β-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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimetabolites / pharmacology
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans / metabolism*
  • Caenorhabditis elegans Proteins / genetics*
  • Caenorhabditis elegans Proteins / metabolism
  • Deoxyglucose / pharmacology
  • Energy Metabolism / genetics*
  • Fatty Acids / metabolism
  • Glycolysis
  • Lipid Peroxidation
  • Membrane Potential, Mitochondrial / drug effects
  • Mitochondria / metabolism
  • Mutation
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism


  • Antimetabolites
  • Caenorhabditis elegans Proteins
  • Fatty Acids
  • RNA, Messenger
  • Reactive Oxygen Species
  • Deoxyglucose