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Glutamine: A novel player in maintaining skeletal strength and body fitness in obese mice

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F25%3A00640575" target="_blank" >RIV/86652036:_____/25:00640575 - isvavai.cz</a>

  • Alternative codes found

    RIV/67985823:_____/25:00640575 RIV/68378050:_____/25:00640575 RIV/00216208:11310/25:10515670

  • Result on the web

    <a href="https://doi.org/10.1016/j.clnu.2025.09.018" target="_blank" >https://doi.org/10.1016/j.clnu.2025.09.018</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.clnu.2025.09.018" target="_blank" >10.1016/j.clnu.2025.09.018</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Glutamine: A novel player in maintaining skeletal strength and body fitness in obese mice

  • Original language description

    Background and aims:Glutamine plays a key role in cellular metabolism and tissue homeostasis. In obesity, circulating glutamine levels decline, accompanied by impaired bone homeostasis and increased fracture risk. While dietary glutamine supplementation shows metabolic benefits, its effects on bone and fat metabolism remain unclear. This study investigates whether glutamine supplementation mitigates obesity-induced alterations in bone and fat metabolism.Methods:C57BL/6J male mice were subjected to a 2-month dietary intervention with either high-fat diet (HFD) or HFD supplemented with glutamine (HFD + G) and low-fat diet (LFD) as a control group. Body weight, fat mass, glucose tolerance, white adipose tissue (WAT) morphology, and bone parameters were analyzed. Functional assays of adipose-derived mesenchymal stem cells (AT-MSCs) and bone marrow stromal cells (BMSCs) assessed metabolic phenotype and differentiation potential. Glutamine turnover was evaluated, and findings were extended to human BMSCs to assess sex-specific patterns of glutaminolysis.Results:Glutamine supplementation attenuated body weight gain, fat mass, and WAT weight, along with improved glucose tolerance compared to HFD-fed mice. In WAT, glutamine reduced adipocyte hypertrophy and inflammation, while in AT-MSCs it suppressed obesity-driven hyper-metabolic phenotype by shifting cells toward quiescence. In bone, glutamine improved bone quality, along with reduced bone marrow adiposity and decreased bone resorption. BMSCs from glutamine-treated mice showed decreased adipogenic and increased osteogenic potential, supported by enhanced glutamine turnover, which maintained the stemness of the cells and reduced the inflammation induced by obesity. In human BMSCs, glutamine metabolism displayed sex-specific differences, underscoring its physiological relevance.Conclusion:Glutamine supplementation improves systemic metabolic health and bone integrity at both the organ and cellular levels, highlighting its potential as a therapeutic strategy for preventing obesity-related metabolic and bone diseases.

  • 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

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2025

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Clinical Nutrition

  • ISSN

    0261-5614

  • e-ISSN

    1532-1983

  • Volume of the periodical

    54

  • Issue of the periodical within the volume

    Nov

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    15

  • Pages from-to

    162-176

  • UT code for WoS article

    001597823500001

  • EID of the result in the Scopus database

    2-s2.0-105020454834