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  1. Article ; Online: On the cutting edge: perspectives in bioenergetics.

    Granath-Panelo, Melia / Krook, Anna / Rutter, Jared / Kajimura, Shingo

    Nature reviews. Endocrinology

    2023  Volume 19, Issue 5, Page(s) 250–251

    MeSH term(s) Humans ; Energy Metabolism
    Language English
    Publishing date 2023-01-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2489381-X
    ISSN 1759-5037 ; 1759-5029
    ISSN (online) 1759-5037
    ISSN 1759-5029
    DOI 10.1038/s41574-023-00820-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6336: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 93: Show issues

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  2. Article ; Online: OXR1 maintains the retromer to delay brain aging under dietary restriction.

    Wilson, Kenneth A / Bar, Sudipta / Dammer, Eric B / Carrera, Enrique M / Hodge, Brian A / Hilsabeck, Tyler A U / Bons, Joanna / Brownridge, George W / Beck, Jennifer N / Rose, Jacob / Granath-Panelo, Melia / Nelson, Christopher S / Qi, Grace / Gerencser, Akos A / Lan, Jianfeng / Afenjar, Alexandra / Chawla, Geetanjali / Brem, Rachel B / Campeau, Philippe M /
    Bellen, Hugo J / Schilling, Birgit / Seyfried, Nicholas T / Ellerby, Lisa M / Kapahi, Pankaj

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 467

    Abstract: Dietary restriction (DR) delays aging, but the mechanism remains unclear. We identified polymorphisms in mtd, the fly homolog of OXR1, which influenced lifespan and mtd expression in response to DR. Knockdown in adulthood inhibited DR-mediated lifespan ... ...

    Abstract Dietary restriction (DR) delays aging, but the mechanism remains unclear. We identified polymorphisms in mtd, the fly homolog of OXR1, which influenced lifespan and mtd expression in response to DR. Knockdown in adulthood inhibited DR-mediated lifespan extension in female flies. We found that mtd/OXR1 expression declines with age and it interacts with the retromer, which regulates trafficking of proteins and lipids. Loss of mtd/OXR1 destabilized the retromer, causing improper protein trafficking and endolysosomal defects. Overexpression of retromer genes or pharmacological restabilization with R55 rescued lifespan and neurodegeneration in mtd-deficient flies and endolysosomal defects in fibroblasts from patients with lethal loss-of-function of OXR1 variants. Multi-omic analyses in flies and humans showed that decreased Mtd/OXR1 is associated with aging and neurological diseases. mtd/OXR1 overexpression rescued age-related visual decline and tauopathy in a fly model. Hence, OXR1 plays a conserved role in preserving retromer function and is critical for neuronal health and longevity.
    MeSH term(s) Humans ; Female ; Aging/genetics ; Longevity/genetics ; Neurons/metabolism ; Nervous System Diseases/metabolism ; Brain/metabolism ; Caloric Restriction ; Mitochondrial Proteins/metabolism
    Chemical Substances OXR1 protein, human ; Mitochondrial Proteins
    Language English
    Publishing date 2024-01-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-44343-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: BCAA-nitrogen flux in brown fat controls metabolic health independent of thermogenesis.

    Verkerke, Anthony R P / Wang, Dandan / Yoshida, Naofumi / Taxin, Zachary H / Shi, Xu / Zheng, Shuning / Li, Yuka / Auger, Christopher / Oikawa, Satoshi / Yook, Jin-Seon / Granath-Panelo, Melia / He, Wentao / Zhang, Guo-Fang / Matsushita, Mami / Saito, Masayuki / Gerszten, Robert E / Mills, Evanna L / Banks, Alexander S / Ishihama, Yasushi /
    White, Phillip J / McGarrah, Robert W / Yoneshiro, Takeshi / Kajimura, Shingo

    Cell

    2024  Volume 187, Issue 10, Page(s) 2359–2374.e18

    Abstract: Brown adipose tissue (BAT) is best known for thermogenesis. Rodent studies demonstrated that enhanced BAT thermogenesis is tightly associated with increased energy expenditure, reduced body weight, and improved glucose homeostasis. However, human BAT is ... ...

    Abstract Brown adipose tissue (BAT) is best known for thermogenesis. Rodent studies demonstrated that enhanced BAT thermogenesis is tightly associated with increased energy expenditure, reduced body weight, and improved glucose homeostasis. However, human BAT is protective against type 2 diabetes, independent of body weight. The mechanism underlying this dissociation remains unclear. Here, we report that impaired mitochondrial catabolism of branched-chain amino acids (BCAAs) in BAT, by deleting mitochondrial BCAA carriers (MBCs), caused systemic insulin resistance without affecting energy expenditure and body weight. Brown adipocytes catabolized BCAA in the mitochondria as nitrogen donors for the biosynthesis of non-essential amino acids and glutathione. Impaired mitochondrial BCAA-nitrogen flux in BAT resulted in increased oxidative stress, decreased hepatic insulin signaling, and decreased circulating BCAA-derived metabolites. A high-fat diet attenuated BCAA-nitrogen flux and metabolite synthesis in BAT, whereas cold-activated BAT enhanced the synthesis. This work uncovers a metabolite-mediated pathway through which BAT controls metabolic health beyond thermogenesis.
    MeSH term(s) Thermogenesis ; Adipose Tissue, Brown/metabolism ; Animals ; Amino Acids, Branched-Chain/metabolism ; Mice ; Nitrogen/metabolism ; Mitochondria/metabolism ; Insulin Resistance ; Male ; Humans ; Energy Metabolism ; Mice, Inbred C57BL ; Oxidative Stress ; Insulin/metabolism ; Diet, High-Fat ; Adipocytes, Brown/metabolism ; Signal Transduction
    Chemical Substances Amino Acids, Branched-Chain ; Nitrogen (N762921K75) ; Insulin
    Language English
    Publishing date 2024-04-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2024.03.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1167: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 58: Show issues

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