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Related Experiment Video

Updated: Jul 27, 2025

Design and Validation of a Volumetric-extrusion Bioprinter for Bioprinting of Soluble Basement Membrane Extract for Translational Research
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Design and Validation of a Volumetric-extrusion Bioprinter for Bioprinting of Soluble Basement Membrane Extract for Translational Research

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Ling Xiao, Dario F De Jesus, Cheng-Wei Ju

    Biorxiv : the Preprint Server for Biology
    |June 9, 2023
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    Summary
    This summary is machine-generated.

    Loss of METTL14 in brown fat enhances insulin sensitivity by altering secreted lipids like PGE2 and PGF2a. This inter-organ communication improves metabolic health independently of thermogenesis.

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    Area of Science:

    • Metabolic Regulation
    • Adipose Tissue Biology
    • Epigenetics

    Background:

    • Brown adipose tissue (BAT) secretes signaling lipids to regulate systemic metabolism.
    • N6-methyladenosine (m6A) modification influences BAT function, including adipogenesis and energy expenditure.
    • The role of m6A in BAT-secreted factors and their impact on systemic insulin sensitivity remains largely unexplored.

    Approach:

    • Investigated the function of METTL14, an m6A methyltransferase, in BAT.
    • Utilized lipidomics to identify key secreted molecules in METTL14 knockout (KO) BAT.
    • Administered identified lipids to diet-induced obese mice to assess insulin sensitivity.
    • Examined the molecular mechanisms of m6A-mediated transcript regulation in brown adipocytes.

    Key Points:

    • METTL14 deficiency in BAT alters the secretome, promoting inter-organ communication and improving systemic insulin sensitivity.
    • Prostaglandin E2 (PGE2) and Prostaglandin F2a (PGF2a) were identified as key BAT-secreted insulin sensitizers.
    • METTL14-mediated m6A installation promotes the decay of transcripts encoding prostaglandin synthases via YTHDF2/3.

    Conclusions:

    • METTL14-dependent m6A modification of BAT secretome regulates systemic insulin sensitivity.
    • PGE2 and PGF2a act as crucial mediators of improved insulin sensitivity in METTL14-deficient states.
    • Targeting METTL14 in BAT presents a potential therapeutic strategy for enhancing systemic insulin sensitivity.