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Interaction between hormone-sensitive lipase and ChREBP in fat cells controls insulin sensitivity

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F19%3A43919417" target="_blank" >RIV/00216208:11120/19:43919417 - isvavai.cz</a>

  • Result on the web

    <a href="https://doi.org/10.1038/s42255-018-0007-6" target="_blank" >https://doi.org/10.1038/s42255-018-0007-6</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/s42255-018-0007-6" target="_blank" >10.1038/s42255-018-0007-6</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Interaction between hormone-sensitive lipase and ChREBP in fat cells controls insulin sensitivity

  • Original language description

    Impaired adipose tissue insulin signalling is a critical feature of insulin resistance. Here we identify a pathway linking the lipolytic enzyme hormone-sensitive lipase (HSL) to insulin action via the glucose-responsive transcription factor ChREBP and its target, the fatty acid elongase ELOVL6. Genetic inhibition of HSL in human adipocytes and mouse adipose tissue results in enhanced insulin sensitivity and induction of ELOVL6. ELOVL6 promotes an increase in phospholipid oleic acid, which modifies plasma membrane fluidity and enhances insulin signalling. HSL deficiency-mediated effects are suppressed by gene silencing of ChREBP and ELOVL6. Mechanistically, physical interaction between HSL, independent of lipase activity, and the isoform activated by glucose metabolism ChREBP alpha impairs ChREBP alpha translocation into the nucleus and induction of ChREBP beta, the isoform with high transcriptional activity that is strongly associated with whole-body insulin sensitivity. Targeting the HSL-ChREBP interaction may allow therapeutic strategies for the restoration of insulin sensitivity.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Result continuities

  • Project

  • Continuities

    N - Vyzkumna aktivita podporovana z neverejnych zdroju

Others

  • Publication year

    2019

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Nature Metabolism

  • ISSN

    2522-5812

  • e-ISSN

  • Volume of the periodical

    1

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    14

  • Pages from-to

    133-146

  • UT code for WoS article

    000500725600017

  • EID of the result in the Scopus database

    2-s2.0-85058842115