The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice
Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhang, Xinzhi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Nature B.V. 2022 |
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| Übergeordnetes Werk: |
Enthalten in: Molecular biology reports - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973, 49(2022), 9 vom: 22. Juni, Seite 8641-8649 |
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| Übergeordnetes Werk: |
volume:49 ; year:2022 ; number:9 ; day:22 ; month:06 ; pages:8641-8649 |
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| DOI / URN: |
10.1007/s11033-022-07699-1 |
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| Katalog-ID: |
SPR048049026 |
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| 100 | 1 | |a Zhang, Xinzhi |e verfasserin |4 aut | |
| 245 | 1 | 4 | |a The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice |
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| 520 | |a Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. | ||
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| 650 | 4 | |a SSR128129E (SSR) |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Adipogenesis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Thermogenic capability |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Lin, Hai |4 aut | |
| 700 | 1 | |a Li, Haifang |0 (orcid)0000-0002-2827-5925 |4 aut | |
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10.1007/s11033-022-07699-1 doi (DE-627)SPR048049026 (SPR)s11033-022-07699-1-e DE-627 ger DE-627 rakwb eng Zhang, Xinzhi verfasserin aut The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature B.V. 2022 Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. Fibroblast growth factor receptor (FGFR) antagonist (dpeaa)DE-He213 SSR128129E (SSR) (dpeaa)DE-He213 Fat metabolism (dpeaa)DE-He213 Adipogenesis (dpeaa)DE-He213 Thermogenic capability (dpeaa)DE-He213 Wen, Xin aut Hu, Geng aut Zhang, Qiang aut Sun, Qianying aut Jia, Yanxin aut Liu, Yan aut Lin, Hai aut Li, Haifang (orcid)0000-0002-2827-5925 aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 49(2022), 9 vom: 22. Juni, Seite 8641-8649 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:49 year:2022 number:9 day:22 month:06 pages:8641-8649 https://dx.doi.org/10.1007/s11033-022-07699-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2548 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 49 2022 9 22 06 8641-8649 |
| spelling |
10.1007/s11033-022-07699-1 doi (DE-627)SPR048049026 (SPR)s11033-022-07699-1-e DE-627 ger DE-627 rakwb eng Zhang, Xinzhi verfasserin aut The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature B.V. 2022 Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. Fibroblast growth factor receptor (FGFR) antagonist (dpeaa)DE-He213 SSR128129E (SSR) (dpeaa)DE-He213 Fat metabolism (dpeaa)DE-He213 Adipogenesis (dpeaa)DE-He213 Thermogenic capability (dpeaa)DE-He213 Wen, Xin aut Hu, Geng aut Zhang, Qiang aut Sun, Qianying aut Jia, Yanxin aut Liu, Yan aut Lin, Hai aut Li, Haifang (orcid)0000-0002-2827-5925 aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 49(2022), 9 vom: 22. Juni, Seite 8641-8649 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:49 year:2022 number:9 day:22 month:06 pages:8641-8649 https://dx.doi.org/10.1007/s11033-022-07699-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2548 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 49 2022 9 22 06 8641-8649 |
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10.1007/s11033-022-07699-1 doi (DE-627)SPR048049026 (SPR)s11033-022-07699-1-e DE-627 ger DE-627 rakwb eng Zhang, Xinzhi verfasserin aut The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature B.V. 2022 Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. Fibroblast growth factor receptor (FGFR) antagonist (dpeaa)DE-He213 SSR128129E (SSR) (dpeaa)DE-He213 Fat metabolism (dpeaa)DE-He213 Adipogenesis (dpeaa)DE-He213 Thermogenic capability (dpeaa)DE-He213 Wen, Xin aut Hu, Geng aut Zhang, Qiang aut Sun, Qianying aut Jia, Yanxin aut Liu, Yan aut Lin, Hai aut Li, Haifang (orcid)0000-0002-2827-5925 aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 49(2022), 9 vom: 22. Juni, Seite 8641-8649 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:49 year:2022 number:9 day:22 month:06 pages:8641-8649 https://dx.doi.org/10.1007/s11033-022-07699-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2548 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 49 2022 9 22 06 8641-8649 |
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10.1007/s11033-022-07699-1 doi (DE-627)SPR048049026 (SPR)s11033-022-07699-1-e DE-627 ger DE-627 rakwb eng Zhang, Xinzhi verfasserin aut The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature B.V. 2022 Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. Fibroblast growth factor receptor (FGFR) antagonist (dpeaa)DE-He213 SSR128129E (SSR) (dpeaa)DE-He213 Fat metabolism (dpeaa)DE-He213 Adipogenesis (dpeaa)DE-He213 Thermogenic capability (dpeaa)DE-He213 Wen, Xin aut Hu, Geng aut Zhang, Qiang aut Sun, Qianying aut Jia, Yanxin aut Liu, Yan aut Lin, Hai aut Li, Haifang (orcid)0000-0002-2827-5925 aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 49(2022), 9 vom: 22. Juni, Seite 8641-8649 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:49 year:2022 number:9 day:22 month:06 pages:8641-8649 https://dx.doi.org/10.1007/s11033-022-07699-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2548 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 49 2022 9 22 06 8641-8649 |
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10.1007/s11033-022-07699-1 doi (DE-627)SPR048049026 (SPR)s11033-022-07699-1-e DE-627 ger DE-627 rakwb eng Zhang, Xinzhi verfasserin aut The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature B.V. 2022 Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. Fibroblast growth factor receptor (FGFR) antagonist (dpeaa)DE-He213 SSR128129E (SSR) (dpeaa)DE-He213 Fat metabolism (dpeaa)DE-He213 Adipogenesis (dpeaa)DE-He213 Thermogenic capability (dpeaa)DE-He213 Wen, Xin aut Hu, Geng aut Zhang, Qiang aut Sun, Qianying aut Jia, Yanxin aut Liu, Yan aut Lin, Hai aut Li, Haifang (orcid)0000-0002-2827-5925 aut Enthalten in Molecular biology reports Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 49(2022), 9 vom: 22. Juni, Seite 8641-8649 (DE-627)270930639 (DE-600)1478217-0 1573-4978 nnns volume:49 year:2022 number:9 day:22 month:06 pages:8641-8649 https://dx.doi.org/10.1007/s11033-022-07699-1 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2548 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 49 2022 9 22 06 8641-8649 |
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Fibroblast growth factor receptor (FGFR) antagonist SSR128129E (SSR) Fat metabolism Adipogenesis Thermogenic capability |
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Zhang, Xinzhi @@aut@@ Wen, Xin @@aut@@ Hu, Geng @@aut@@ Zhang, Qiang @@aut@@ Sun, Qianying @@aut@@ Jia, Yanxin @@aut@@ Liu, Yan @@aut@@ Lin, Hai @@aut@@ Li, Haifang @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR048049026</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519100224.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">220910s2022 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s11033-022-07699-1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR048049026</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s11033-022-07699-1-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Zhang, Xinzhi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s), under exclusive licence to Springer Nature B.V. 2022</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. 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Zhang, Xinzhi |
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Zhang, Xinzhi misc Fibroblast growth factor receptor (FGFR) antagonist misc SSR128129E (SSR) misc Fat metabolism misc Adipogenesis misc Thermogenic capability The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice |
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The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice Fibroblast growth factor receptor (FGFR) antagonist (dpeaa)DE-He213 SSR128129E (SSR) (dpeaa)DE-He213 Fat metabolism (dpeaa)DE-He213 Adipogenesis (dpeaa)DE-He213 Thermogenic capability (dpeaa)DE-He213 |
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misc Fibroblast growth factor receptor (FGFR) antagonist misc SSR128129E (SSR) misc Fat metabolism misc Adipogenesis misc Thermogenic capability |
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The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice |
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fibroblast growth factor receptor antagonist ssr128129e inhibits fat accumulation via suppressing adipogenesis in mice |
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The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice |
| abstract |
Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. © The Author(s), under exclusive licence to Springer Nature B.V. 2022 |
| abstractGer |
Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. © The Author(s), under exclusive licence to Springer Nature B.V. 2022 |
| abstract_unstemmed |
Background AS an allosteric inhibitor of fibroblast growth factor receptors (FGFRs), SSR128129E (SSR) extensively inhibits the fibroblast growth factor (FGF) signaling. Given the metabolic importance of FGFs and the global epidemic of obesity, we explored the effect of SSR on fat metabolism. Methods and results Three-week-old male mice were administered intragastrically with SSR (30 mg/kg/day) or PBS for 5 weeks. The effects of SSR on white and brown fat metabolism were investigated by respiratory metabolic monitoring, histological assessment and molecular analysis. Results indicated that SSR administration significantly reduced the body weight gain and the fat content of mice. SSR did not increase, but decreased the thermogenic capability of both brown and white fat. However, SSR markedly suppressed adipogenesis of adipose tissues. Further study demonstrated the involvement of ERK signaling in the action of SSR. Conclusions SSR may be a promising drug candidate for the prevention of obesity via suppressing adipogenesis. However, the influence of SSR on thermogenesis in humans should be further investigated before its clinical application. © The Author(s), under exclusive licence to Springer Nature B.V. 2022 |
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The fibroblast growth factor receptor antagonist SSR128129E inhibits fat accumulation via suppressing adipogenesis in mice |
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https://dx.doi.org/10.1007/s11033-022-07699-1 |
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Wen, Xin Hu, Geng Zhang, Qiang Sun, Qianying Jia, Yanxin Liu, Yan Lin, Hai Li, Haifang |
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Wen, Xin Hu, Geng Zhang, Qiang Sun, Qianying Jia, Yanxin Liu, Yan Lin, Hai Li, Haifang |
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| score |
7.400487 |