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

Identifikátory výsledku

  • Kód výsledku v 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>

  • Nalezeny alternativní kódy

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

  • Výsledek na webu

    <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>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

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

  • Popis výsledku v původním jazyce

    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.

  • Název v anglickém jazyce

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

  • Popis výsledku anglicky

    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.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Návaznosti výsledku

  • Projekt

    Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2025

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Clinical Nutrition

  • ISSN

    0261-5614

  • e-ISSN

    1532-1983

  • Svazek periodika

    54

  • Číslo periodika v rámci svazku

    Nov

  • Stát vydavatele periodika

    GB - Spojené království Velké Británie a Severního Irska

  • Počet stran výsledku

    15

  • Strana od-do

    162-176

  • Kód UT WoS článku

    001597823500001

  • EID výsledku v databázi Scopus

    2-s2.0-105020454834