ArticleBMB reports2014
Mutation of the lbp-5 gene alters metabolic output in Caenorhabditis elegans.
Article in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 8 citations in OpenAlex.
- Application ofInternational journal of molecular sciences · 2023Review
- Adaptation of AMPK-mTOR-signal pathways and lipid metabolism in response to low- and high-level rapeseed meal diet in Chinese perch (Siniperca chuatsi).Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2021Article
- In Vivo Microbial Coevolution Favors Host Protection and Plastic Downregulation of Immunity.Molecular biology and evolution · 2021Article
- A comparison of the mitochondrial proteome and lipidome in the mouse and long-lived Pipistrelle bats.Aging · 2019Article
- Identification of key pathways and metabolic fingerprints of longevity in C. elegans.Experimental gerontology · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
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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 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.
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