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mice, adko, fig, ctrl, mitochondrial, pubmed, oxphos, adipose, article, hfd, weeks, gdf, google, scholar, esm, insulin, cas, fgf, iwat, weekold, expression, fed, tissue, glucose, ewat, protein, obesity, systemic, energy, control, homeostasis, adgko, body, function, metabolic, adfko, mass, data, adipocytes, adipocyte, resistance, uprmt, ncdfed, central, crif, metabolism, wat, mitokines, ncd, adipocytespecific,

Topics {✒️}

hyon-seung yi hyun jin kim high-fat diet conditions adipocyte-specific crif1 knockout adipocyte-specific pgc-1β impaired oxphos-mediated induction treated 3 t3-l1 adipocytes differentiated 3 t3-l1 adipocytes bn-page analysis due tissue-specific knockout mice energy-dependent proton ejection alleviate diet-induced obesity exacerbate diet-induced obesity fatty acid metabolism adipose tissue-specific gdf15 bn-page analysis revealed hyun jung hong adipocyte mitochondria play real-time pcr quantification ppargamma agonist-induced adipogenesis systemic energy metabolism improves systemic metabolism high-fat diet min jeong ryu mice lacking pgc-1beta joon young chang brown adipose tissue minho shong oxphos dysfunction-induced uprmt related subjects full access systemic glucose metabolism adipoq-cre transgenic mice reduced oxidative capacity affected macrophage polarisation adipocyte-specific impairment adipocyte-specific crif1 normal glucose metabolism systemic energy homeostasis ectopic ucp1 overexpression wild-type control mice decreased adipocyte oxphos chul-ho lee inguinal adipose tissue transcriptional profile mitochondrial stress response hyo kyun chung oxidative phosphorylation polypeptides oxidative phosphorylation disorders privacy choices/manage cookies

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         headline:An adipocyte-specific defect in oxidative phosphorylation increases systemic energy expenditure and protects against diet-induced obesity in mouse models
         description:Mitochondrial oxidative phosphorylation (OxPhos) is essential for energy production and survival. However, the tissue-specific and systemic metabolic effects of OxPhos function in adipocytes remain incompletely understood. We used adipocyte-specific Crif1 (also known as Gadd45gip1) knockout (AdKO) mice with decreased adipocyte OxPhos function. AdKO mice fed a normal chow or high-fat diet were evaluated for glucose homeostasis, weight gain and energy expenditure (EE). RNA sequencing of adipose tissues was used to identify the key mitokines affected in AdKO mice, which included fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15). For in vitro analysis, doxycycline was used to pharmacologically decrease OxPhos in 3T3L1 adipocytes. To identify the effects of GDF15 and FGF21 on the metabolic phenotype of AdKO mice, we generated AdKO mice with global Gdf15 knockout (AdGKO) or global Fgf21 knockout (AdFKO). Under high-fat diet conditions, AdKO mice were resistant to weight gain and exhibited higher EE and improved glucose tolerance. In vitro pharmacological and in vivo genetic inhibition of OxPhos in adipocytes significantly upregulated mitochondrial unfolded protein response-related genes and secretion of mitokines such as GDF15 and FGF21. We evaluated the metabolic phenotypes of AdGKO and AdFKO mice, revealing that GDF15 and FGF21 differentially regulated energy homeostasis in AdKO mice. Both mitokines had beneficial effects on obesity and insulin resistance in the context of decreased adipocyte OxPhos, but only GDF15 regulated EE in AdKO mice. The present study demonstrated that the adipose tissue adaptive mitochondrial stress response affected systemic energy homeostasis via cell-autonomous and non-cell-autonomous pathways. We identified novel roles for adipose OxPhos and adipo-mitokines in the regulation of systemic glucose homeostasis and EE, which facilitated adaptation of an organism to local mitochondrial stress.
         datePublished:2020-01-10T00:00:00Z
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         keywords:
            Adipose tissue
            Energy metabolism
            Insulin resistance
            Mitochondria
            Mitokine
            Internal Medicine
            Metabolic Diseases
            Human Physiology
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      headline:An adipocyte-specific defect in oxidative phosphorylation increases systemic energy expenditure and protects against diet-induced obesity in mouse models
      description:Mitochondrial oxidative phosphorylation (OxPhos) is essential for energy production and survival. However, the tissue-specific and systemic metabolic effects of OxPhos function in adipocytes remain incompletely understood. We used adipocyte-specific Crif1 (also known as Gadd45gip1) knockout (AdKO) mice with decreased adipocyte OxPhos function. AdKO mice fed a normal chow or high-fat diet were evaluated for glucose homeostasis, weight gain and energy expenditure (EE). RNA sequencing of adipose tissues was used to identify the key mitokines affected in AdKO mice, which included fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15). For in vitro analysis, doxycycline was used to pharmacologically decrease OxPhos in 3T3L1 adipocytes. To identify the effects of GDF15 and FGF21 on the metabolic phenotype of AdKO mice, we generated AdKO mice with global Gdf15 knockout (AdGKO) or global Fgf21 knockout (AdFKO). Under high-fat diet conditions, AdKO mice were resistant to weight gain and exhibited higher EE and improved glucose tolerance. In vitro pharmacological and in vivo genetic inhibition of OxPhos in adipocytes significantly upregulated mitochondrial unfolded protein response-related genes and secretion of mitokines such as GDF15 and FGF21. We evaluated the metabolic phenotypes of AdGKO and AdFKO mice, revealing that GDF15 and FGF21 differentially regulated energy homeostasis in AdKO mice. Both mitokines had beneficial effects on obesity and insulin resistance in the context of decreased adipocyte OxPhos, but only GDF15 regulated EE in AdKO mice. The present study demonstrated that the adipose tissue adaptive mitochondrial stress response affected systemic energy homeostasis via cell-autonomous and non-cell-autonomous pathways. We identified novel roles for adipose OxPhos and adipo-mitokines in the regulation of systemic glucose homeostasis and EE, which facilitated adaptation of an organism to local mitochondrial stress.
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      pageEnd:852
      sameAs:https://doi.org/10.1007/s00125-019-05082-7
      keywords:
         Adipose tissue
         Energy metabolism
         Insulin resistance
         Mitochondria
         Mitokine
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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            address:
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            address:
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      affiliation:
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            address:
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            address:
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            name:Chungnam National University Hospital
            address:
               name:Department of Internal Medicine, Chungnam National University Hospital, Daejeon, South Korea
               type:PostalAddress
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      name:Minho Shong
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      affiliation:
            name:Chungnam National University School of Medicine
            address:
               name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
               type:PostalAddress
            type:Organization
            name:Chungnam National University Hospital
            address:
               name:Department of Internal Medicine, Chungnam National University Hospital, Daejeon, South Korea
               type:PostalAddress
            type:Organization
      email:[email protected]
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      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Medical Science, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Medical Science, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Internal Medicine, Chungnam National University Hospital, Daejeon, South Korea
      name:Department of Biochemistry, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Medical Science, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Medical Science, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Internal Medicine, Chungnam National University Hospital, Daejeon, South Korea
      name:Animal Model Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, South Korea
      name:Science for Life Laboratory, KTH – Royal Institute of Technology, Stockholm, Sweden
      name:Centre for Host–Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, London, UK
      name:Department of Internal Medicine, Chungnam National University Hospital, Daejeon, South Korea
      name:Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon, South Korea
      name:Department of Internal Medicine, Chungnam National University Hospital, Daejeon, South Korea

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