Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance
Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-m...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sun, Yunyan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s) 2023 |
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| Übergeordnetes Werk: |
Enthalten in: Cellular and molecular life sciences - Cham (ZG) : Springer International Publishing AG, 1997, 80(2023), 3 vom: 13. Feb. |
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| Übergeordnetes Werk: |
volume:80 ; year:2023 ; number:3 ; day:13 ; month:02 |
| Links: |
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| DOI / URN: |
10.1007/s00018-023-04707-w |
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| Katalog-ID: |
SPR049586254 |
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| 100 | 1 | |a Sun, Yunyan |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance |
| 264 | 1 | |c 2023 | |
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| 520 | |a Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. | ||
| 650 | 4 | |a Visceral adipose tissue |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Dendritic cells |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Macrophages |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a IL-17A |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a IFN-γ |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Liver kinase B1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a High-fat-diet-induced obesity |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Wang, Bing |4 aut | |
| 700 | 1 | |a Hu, Qianwen |4 aut | |
| 700 | 1 | |a Zhang, Haixiao |4 aut | |
| 700 | 1 | |a Lai, Xun |4 aut | |
| 700 | 1 | |a Wang, Tier |4 aut | |
| 700 | 1 | |a Zhao, Chunxiao |4 aut | |
| 700 | 1 | |a Wang, Jiali |4 aut | |
| 700 | 1 | |a Zhang, Xi |4 aut | |
| 700 | 1 | |a Niu, Qing |4 aut | |
| 700 | 1 | |a He, Baolin |4 aut | |
| 700 | 1 | |a Jiang, Erlie |4 aut | |
| 700 | 1 | |a Shi, Mingxia |4 aut | |
| 700 | 1 | |a Feng, Xiaoming |4 aut | |
| 700 | 1 | |a Luo, Yuechen |0 (orcid)0000-0001-8912-1818 |4 aut | |
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10.1007/s00018-023-04707-w doi (DE-627)SPR049586254 (SPR)s00018-023-04707-w-e DE-627 ger DE-627 rakwb eng Sun, Yunyan verfasserin aut Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. Visceral adipose tissue (dpeaa)DE-He213 Dendritic cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 T cells (dpeaa)DE-He213 IL-17A (dpeaa)DE-He213 IFN-γ (dpeaa)DE-He213 Liver kinase B1 (dpeaa)DE-He213 High-fat-diet-induced obesity (dpeaa)DE-He213 Wang, Bing aut Hu, Qianwen aut Zhang, Haixiao aut Lai, Xun aut Wang, Tier aut Zhao, Chunxiao aut Wang, Jiali aut Zhang, Xi aut Niu, Qing aut He, Baolin aut Jiang, Erlie aut Shi, Mingxia aut Feng, Xiaoming aut Luo, Yuechen (orcid)0000-0001-8912-1818 aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 80(2023), 3 vom: 13. Feb. (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:80 year:2023 number:3 day:13 month:02 https://dx.doi.org/10.1007/s00018-023-04707-w kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 80 2023 3 13 02 |
| spelling |
10.1007/s00018-023-04707-w doi (DE-627)SPR049586254 (SPR)s00018-023-04707-w-e DE-627 ger DE-627 rakwb eng Sun, Yunyan verfasserin aut Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. Visceral adipose tissue (dpeaa)DE-He213 Dendritic cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 T cells (dpeaa)DE-He213 IL-17A (dpeaa)DE-He213 IFN-γ (dpeaa)DE-He213 Liver kinase B1 (dpeaa)DE-He213 High-fat-diet-induced obesity (dpeaa)DE-He213 Wang, Bing aut Hu, Qianwen aut Zhang, Haixiao aut Lai, Xun aut Wang, Tier aut Zhao, Chunxiao aut Wang, Jiali aut Zhang, Xi aut Niu, Qing aut He, Baolin aut Jiang, Erlie aut Shi, Mingxia aut Feng, Xiaoming aut Luo, Yuechen (orcid)0000-0001-8912-1818 aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 80(2023), 3 vom: 13. Feb. (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:80 year:2023 number:3 day:13 month:02 https://dx.doi.org/10.1007/s00018-023-04707-w kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 80 2023 3 13 02 |
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10.1007/s00018-023-04707-w doi (DE-627)SPR049586254 (SPR)s00018-023-04707-w-e DE-627 ger DE-627 rakwb eng Sun, Yunyan verfasserin aut Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. Visceral adipose tissue (dpeaa)DE-He213 Dendritic cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 T cells (dpeaa)DE-He213 IL-17A (dpeaa)DE-He213 IFN-γ (dpeaa)DE-He213 Liver kinase B1 (dpeaa)DE-He213 High-fat-diet-induced obesity (dpeaa)DE-He213 Wang, Bing aut Hu, Qianwen aut Zhang, Haixiao aut Lai, Xun aut Wang, Tier aut Zhao, Chunxiao aut Wang, Jiali aut Zhang, Xi aut Niu, Qing aut He, Baolin aut Jiang, Erlie aut Shi, Mingxia aut Feng, Xiaoming aut Luo, Yuechen (orcid)0000-0001-8912-1818 aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 80(2023), 3 vom: 13. Feb. (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:80 year:2023 number:3 day:13 month:02 https://dx.doi.org/10.1007/s00018-023-04707-w kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 80 2023 3 13 02 |
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10.1007/s00018-023-04707-w doi (DE-627)SPR049586254 (SPR)s00018-023-04707-w-e DE-627 ger DE-627 rakwb eng Sun, Yunyan verfasserin aut Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. Visceral adipose tissue (dpeaa)DE-He213 Dendritic cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 T cells (dpeaa)DE-He213 IL-17A (dpeaa)DE-He213 IFN-γ (dpeaa)DE-He213 Liver kinase B1 (dpeaa)DE-He213 High-fat-diet-induced obesity (dpeaa)DE-He213 Wang, Bing aut Hu, Qianwen aut Zhang, Haixiao aut Lai, Xun aut Wang, Tier aut Zhao, Chunxiao aut Wang, Jiali aut Zhang, Xi aut Niu, Qing aut He, Baolin aut Jiang, Erlie aut Shi, Mingxia aut Feng, Xiaoming aut Luo, Yuechen (orcid)0000-0001-8912-1818 aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 80(2023), 3 vom: 13. Feb. (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:80 year:2023 number:3 day:13 month:02 https://dx.doi.org/10.1007/s00018-023-04707-w kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 80 2023 3 13 02 |
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10.1007/s00018-023-04707-w doi (DE-627)SPR049586254 (SPR)s00018-023-04707-w-e DE-627 ger DE-627 rakwb eng Sun, Yunyan verfasserin aut Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. Visceral adipose tissue (dpeaa)DE-He213 Dendritic cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 T cells (dpeaa)DE-He213 IL-17A (dpeaa)DE-He213 IFN-γ (dpeaa)DE-He213 Liver kinase B1 (dpeaa)DE-He213 High-fat-diet-induced obesity (dpeaa)DE-He213 Wang, Bing aut Hu, Qianwen aut Zhang, Haixiao aut Lai, Xun aut Wang, Tier aut Zhao, Chunxiao aut Wang, Jiali aut Zhang, Xi aut Niu, Qing aut He, Baolin aut Jiang, Erlie aut Shi, Mingxia aut Feng, Xiaoming aut Luo, Yuechen (orcid)0000-0001-8912-1818 aut Enthalten in Cellular and molecular life sciences Cham (ZG) : Springer International Publishing AG, 1997 80(2023), 3 vom: 13. Feb. (DE-627)253390524 (DE-600)1458497-9 1420-9071 nnns volume:80 year:2023 number:3 day:13 month:02 https://dx.doi.org/10.1007/s00018-023-04707-w kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 80 2023 3 13 02 |
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Enthalten in Cellular and molecular life sciences 80(2023), 3 vom: 13. Feb. volume:80 year:2023 number:3 day:13 month:02 |
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Visceral adipose tissue Dendritic cells Macrophages T cells IL-17A IFN-γ Liver kinase B1 High-fat-diet-induced obesity |
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Sun, Yunyan @@aut@@ Wang, Bing @@aut@@ Hu, Qianwen @@aut@@ Zhang, Haixiao @@aut@@ Lai, Xun @@aut@@ Wang, Tier @@aut@@ Zhao, Chunxiao @@aut@@ Wang, Jiali @@aut@@ Zhang, Xi @@aut@@ Niu, Qing @@aut@@ He, Baolin @@aut@@ Jiang, Erlie @@aut@@ Shi, Mingxia @@aut@@ Feng, Xiaoming @@aut@@ Luo, Yuechen @@aut@@ |
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However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. 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|
| author |
Sun, Yunyan |
| spellingShingle |
Sun, Yunyan misc Visceral adipose tissue misc Dendritic cells misc Macrophages misc T cells misc IL-17A misc IFN-γ misc Liver kinase B1 misc High-fat-diet-induced obesity Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance |
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Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance Visceral adipose tissue (dpeaa)DE-He213 Dendritic cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 T cells (dpeaa)DE-He213 IL-17A (dpeaa)DE-He213 IFN-γ (dpeaa)DE-He213 Liver kinase B1 (dpeaa)DE-He213 High-fat-diet-induced obesity (dpeaa)DE-He213 |
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misc Visceral adipose tissue misc Dendritic cells misc Macrophages misc T cells misc IL-17A misc IFN-γ misc Liver kinase B1 misc High-fat-diet-induced obesity |
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misc Visceral adipose tissue misc Dendritic cells misc Macrophages misc T cells misc IL-17A misc IFN-γ misc Liver kinase B1 misc High-fat-diet-induced obesity |
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misc Visceral adipose tissue misc Dendritic cells misc Macrophages misc T cells misc IL-17A misc IFN-γ misc Liver kinase B1 misc High-fat-diet-induced obesity |
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Cellular and molecular life sciences |
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Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance |
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Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance |
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Sun, Yunyan |
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Sun, Yunyan Wang, Bing Hu, Qianwen Zhang, Haixiao Lai, Xun Wang, Tier Zhao, Chunxiao Wang, Jiali Zhang, Xi Niu, Qing He, Baolin Jiang, Erlie Shi, Mingxia Feng, Xiaoming Luo, Yuechen |
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Elektronische Aufsätze |
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Sun, Yunyan |
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loss of lkb1 in $ cd11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and il-17/ifn-γ imbalance |
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Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance |
| abstract |
Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. © The Author(s) 2023 |
| abstractGer |
Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. © The Author(s) 2023 |
| abstract_unstemmed |
Abstract Adipose tissue $ CD11c^{+} $ myeloid cell is an independent risk factor associated with obesity and metabolic disorders. However, the underlying molecular basis remains elusive. Here, we demonstrated that liver kinase B1 (Lkb1), a key bioenergetic sensor, is involved in $ CD11c^{+} $ cell-mediated immune responses in diet-induced obesity. Loss of Lkb1 in $ CD11c^{+} $ cells results in obesity resistance but lower glucose tolerance, which accompanies tissue-specific immune abnormalities. The accumulation and CD80’s expression of Lkb1 deficient adipose-tissue specific dendritic cells but not macrophages is restrained. Additionally, the balance of IL-17A and IFN-γ remarkably tips towards the latter in fat T cells and $ CD11c^{−} $ macrophages. Mechanistically, IFN-γ promotes apoptosis of preadipocytes and inhibits their adipogenesis while IL-17A promotes the adipogenesis in vitro, which might account in part for the fat gain resistant phenotype. In summary, these findings reveal that Lkb1 is essential for fat $ CD11c^{+} $ dendritic cells responding to HFD exposure and provides new insights into the IL-17A/IFN-γ balance in HFD-induced obesity. © The Author(s) 2023 |
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Loss of Lkb1 in $ CD11c^{+} $ myeloid cells protects mice from diet-induced obesity while enhancing glucose intolerance and IL-17/IFN-γ imbalance |
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Wang, Bing Hu, Qianwen Zhang, Haixiao Lai, Xun Wang, Tier Zhao, Chunxiao Wang, Jiali Zhang, Xi Niu, Qing He, Baolin Jiang, Erlie Shi, Mingxia Feng, Xiaoming Luo, Yuechen |
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Wang, Bing Hu, Qianwen Zhang, Haixiao Lai, Xun Wang, Tier Zhao, Chunxiao Wang, Jiali Zhang, Xi Niu, Qing He, Baolin Jiang, Erlie Shi, Mingxia Feng, Xiaoming Luo, Yuechen |
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| score |
7.400769 |