1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM
Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhou, Zhengyu [verfasserIn] Zhang, Lewen [verfasserIn] Wei, Xun [verfasserIn] Wang, Aiqing [verfasserIn] Hu, Yudie [verfasserIn] Xiao, Min [verfasserIn] Zheng, Yuxuan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2024 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Endocrine - Springer US, 1995, 85(2024), 3 vom: 24. Apr., Seite 1193-1205 |
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| Übergeordnetes Werk: |
volume:85 ; year:2024 ; number:3 ; day:24 ; month:04 ; pages:1193-1205 |
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| DOI / URN: |
10.1007/s12020-024-03833-0 |
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| Katalog-ID: |
SPR056928475 |
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| 520 | |a Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. | ||
| 520 | |a Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. | ||
| 650 | 4 | |a Type 2 diabetes mellitus |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Vitamin D |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Pancreatic stellate cells |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Fibrosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Inflammation. |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Zhang, Lewen |e verfasserin |4 aut | |
| 700 | 1 | |a Wei, Xun |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Aiqing |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Yudie |e verfasserin |4 aut | |
| 700 | 1 | |a Xiao, Min |e verfasserin |4 aut | |
| 700 | 1 | |a Zheng, Yuxuan |e verfasserin |4 aut | |
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10.1007/s12020-024-03833-0 doi (DE-627)SPR056928475 (SPR)s12020-024-03833-0-e DE-627 ger DE-627 rakwb eng 610 VZ 44.89 bkl Zhou, Zhengyu verfasserin aut 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. Type 2 diabetes mellitus (dpeaa)DE-He213 Vitamin D (dpeaa)DE-He213 Pancreatic stellate cells (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Inflammation. (dpeaa)DE-He213 Zhang, Lewen verfasserin aut Wei, Xun verfasserin aut Wang, Aiqing verfasserin aut Hu, Yudie verfasserin aut Xiao, Min verfasserin aut Zheng, Yuxuan verfasserin aut Enthalten in Endocrine Springer US, 1995 85(2024), 3 vom: 24. Apr., Seite 1193-1205 (DE-627)343970171 (DE-600)2074043-8 1559-0100 nnns volume:85 year:2024 number:3 day:24 month:04 pages:1193-1205 https://dx.doi.org/10.1007/s12020-024-03833-0 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 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_65 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_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 44.89 VZ AR 85 2024 3 24 04 1193-1205 |
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10.1007/s12020-024-03833-0 doi (DE-627)SPR056928475 (SPR)s12020-024-03833-0-e DE-627 ger DE-627 rakwb eng 610 VZ 44.89 bkl Zhou, Zhengyu verfasserin aut 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. Type 2 diabetes mellitus (dpeaa)DE-He213 Vitamin D (dpeaa)DE-He213 Pancreatic stellate cells (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Inflammation. (dpeaa)DE-He213 Zhang, Lewen verfasserin aut Wei, Xun verfasserin aut Wang, Aiqing verfasserin aut Hu, Yudie verfasserin aut Xiao, Min verfasserin aut Zheng, Yuxuan verfasserin aut Enthalten in Endocrine Springer US, 1995 85(2024), 3 vom: 24. Apr., Seite 1193-1205 (DE-627)343970171 (DE-600)2074043-8 1559-0100 nnns volume:85 year:2024 number:3 day:24 month:04 pages:1193-1205 https://dx.doi.org/10.1007/s12020-024-03833-0 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 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_65 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_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 44.89 VZ AR 85 2024 3 24 04 1193-1205 |
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10.1007/s12020-024-03833-0 doi (DE-627)SPR056928475 (SPR)s12020-024-03833-0-e DE-627 ger DE-627 rakwb eng 610 VZ 44.89 bkl Zhou, Zhengyu verfasserin aut 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. Type 2 diabetes mellitus (dpeaa)DE-He213 Vitamin D (dpeaa)DE-He213 Pancreatic stellate cells (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Inflammation. (dpeaa)DE-He213 Zhang, Lewen verfasserin aut Wei, Xun verfasserin aut Wang, Aiqing verfasserin aut Hu, Yudie verfasserin aut Xiao, Min verfasserin aut Zheng, Yuxuan verfasserin aut Enthalten in Endocrine Springer US, 1995 85(2024), 3 vom: 24. Apr., Seite 1193-1205 (DE-627)343970171 (DE-600)2074043-8 1559-0100 nnns volume:85 year:2024 number:3 day:24 month:04 pages:1193-1205 https://dx.doi.org/10.1007/s12020-024-03833-0 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 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_65 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_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 44.89 VZ AR 85 2024 3 24 04 1193-1205 |
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10.1007/s12020-024-03833-0 doi (DE-627)SPR056928475 (SPR)s12020-024-03833-0-e DE-627 ger DE-627 rakwb eng 610 VZ 44.89 bkl Zhou, Zhengyu verfasserin aut 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. Type 2 diabetes mellitus (dpeaa)DE-He213 Vitamin D (dpeaa)DE-He213 Pancreatic stellate cells (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Inflammation. (dpeaa)DE-He213 Zhang, Lewen verfasserin aut Wei, Xun verfasserin aut Wang, Aiqing verfasserin aut Hu, Yudie verfasserin aut Xiao, Min verfasserin aut Zheng, Yuxuan verfasserin aut Enthalten in Endocrine Springer US, 1995 85(2024), 3 vom: 24. Apr., Seite 1193-1205 (DE-627)343970171 (DE-600)2074043-8 1559-0100 nnns volume:85 year:2024 number:3 day:24 month:04 pages:1193-1205 https://dx.doi.org/10.1007/s12020-024-03833-0 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 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_65 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_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 44.89 VZ AR 85 2024 3 24 04 1193-1205 |
| allfieldsSound |
10.1007/s12020-024-03833-0 doi (DE-627)SPR056928475 (SPR)s12020-024-03833-0-e DE-627 ger DE-627 rakwb eng 610 VZ 44.89 bkl Zhou, Zhengyu verfasserin aut 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. Type 2 diabetes mellitus (dpeaa)DE-He213 Vitamin D (dpeaa)DE-He213 Pancreatic stellate cells (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Inflammation. (dpeaa)DE-He213 Zhang, Lewen verfasserin aut Wei, Xun verfasserin aut Wang, Aiqing verfasserin aut Hu, Yudie verfasserin aut Xiao, Min verfasserin aut Zheng, Yuxuan verfasserin aut Enthalten in Endocrine Springer US, 1995 85(2024), 3 vom: 24. Apr., Seite 1193-1205 (DE-627)343970171 (DE-600)2074043-8 1559-0100 nnns volume:85 year:2024 number:3 day:24 month:04 pages:1193-1205 https://dx.doi.org/10.1007/s12020-024-03833-0 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 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_65 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_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 44.89 VZ AR 85 2024 3 24 04 1193-1205 |
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Enthalten in Endocrine 85(2024), 3 vom: 24. Apr., Seite 1193-1205 volume:85 year:2024 number:3 day:24 month:04 pages:1193-1205 |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR056928475</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240811064640.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">240811s2024 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s12020-024-03833-0</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR056928475</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12020-024-03833-0-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="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.89</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Zhou, Zhengyu</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2024</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 Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Type 2 diabetes mellitus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Vitamin D</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Pancreatic stellate cells</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Fibrosis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Inflammation.</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Lewen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wei, Xun</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Aiqing</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hu, Yudie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xiao, Min</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zheng, Yuxuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Endocrine</subfield><subfield code="d">Springer US, 1995</subfield><subfield code="g">85(2024), 3 vom: 24. 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Zhou, Zhengyu |
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Zhou, Zhengyu ddc 610 bkl 44.89 misc Type 2 diabetes mellitus misc Vitamin D misc Pancreatic stellate cells misc Fibrosis misc Inflammation. 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM |
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610 VZ 44.89 bkl 1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM Type 2 diabetes mellitus (dpeaa)DE-He213 Vitamin D (dpeaa)DE-He213 Pancreatic stellate cells (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Inflammation. (dpeaa)DE-He213 |
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ddc 610 bkl 44.89 misc Type 2 diabetes mellitus misc Vitamin D misc Pancreatic stellate cells misc Fibrosis misc Inflammation. |
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ddc 610 bkl 44.89 misc Type 2 diabetes mellitus misc Vitamin D misc Pancreatic stellate cells misc Fibrosis misc Inflammation. |
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1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM |
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1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM |
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1,25(oh)2$ d_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in t2dm |
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1,25(OH)2$ D_{3} $ inhibits pancreatic stellate cells activation and promotes insulin secretion in T2DM |
| abstract |
Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Purpose To evaluate the effect and mechanism of 1,25(OH)2$ D_{3} $ on pancreatic stellate cells (PSCs) in type 2 diabetes mellitus (T2DM). Methods A mouse model of T2DM was successfully established by high-fat diet (HFD) /streptozotocin (STZ) and administered 1,25(OH)2$ D_{3} $ for 3 weeks. Fasting blood glucose (FBG), glycated hemoglobin A1c (GHbA1c), insulin (INS) and glucose tolerance were measured. Histopathology changes and fibrosis of pancreas were examined by hematoxylin and eosin staining and Masson staining. Mouse PSCs were extracted, co-cultured with mouse insulinoma β cells (MIN6 cells) and treated with 1,25(OH)2$ D_{3} $. ELISA detection of inflammatory factor expression. Tissue reactive oxygen species (ROS) levels were also measured. Immunofluorescence or Western blotting were used to measure fibrosis and inflammation-related protein expression. Results PSCs activation and islets fibrosis in T2DM mice. Elevated blood glucose was accompanied by significant increases in serum inflammatory cytokines and tissue ROS levels. 1,25(OH)2$ D_{3} $ attenuated islet fibrosis by reducing hyperglycemia, ROS levels, and inflammatory factors expression. Additionally, the co-culture system confirmed that 1,25(OH)2$ D_{3} $ inhibited PSCs activation, reduced the secretion of pro-inflammatory cytokines, down-regulated the expression of fibrosis and inflammation-related proteins, and promoted insulin secretion. Conclusion Our findings identify that PSCs activation contributes to islet fibrosis and β-cell dysfunction. 1,25(OH)2$ D_{3} $ exerts beneficial effects on T2DM potentially by inhibiting PSCs activation and inflammatory response, highlighting promising control strategies of T2DM by vitamin D. Graphical Abstract Fig. 7 Molecular mechanism of 1,25(OH)2$ D_{3} $ in β cell damage following PSCs activation in T2DM mice. Highlights PSCs activation leads to islet fibrosis in T2DM mice.TGF- β, IL-1 β, TNF-α, ROS induce PSCs activation, thereby inhibiting MIN6 cell proliferation and function.1,25(OH)2$ D_{3} $ inhibits PSCs activation by downregulating the expression of factors such as TGF-β, protecting β cell function. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| score |
7.398425 |