High-fat diet unveils an enhancer element at the
Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonl...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Vastolo, Viviana [verfasserIn] Nettore, Immacolata Cristina [verfasserIn] Ciccarelli, Marco [verfasserIn] Albano, Luigi [verfasserIn] Raciti, Gregory Alexander [verfasserIn] Longo, Michele [verfasserIn] Beguinot, Francesco [verfasserIn] Ungaro, Paola [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Metabolism - Orlando, Fla. : Elsevier, 1964, 87, Seite 70-79 |
|---|---|
| Übergeordnetes Werk: |
volume:87 ; pages:70-79 |
| DOI / URN: |
10.1016/j.metabol.2018.06.001 |
|---|
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ELV000682500 |
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| 024 | 7 | |a 10.1016/j.metabol.2018.06.001 |2 doi | |
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| 100 | 1 | |a Vastolo, Viviana |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a High-fat diet unveils an enhancer element at the |
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| 520 | |a Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. | ||
| 650 | 4 | |a Chromatin remodelling | |
| 650 | 4 | |a Enhancer | |
| 650 | 4 | |a Metabolic memory | |
| 650 | 4 | |a Type 2 diabetes | |
| 700 | 1 | |a Nettore, Immacolata Cristina |e verfasserin |4 aut | |
| 700 | 1 | |a Ciccarelli, Marco |e verfasserin |4 aut | |
| 700 | 1 | |a Albano, Luigi |e verfasserin |4 aut | |
| 700 | 1 | |a Raciti, Gregory Alexander |e verfasserin |4 aut | |
| 700 | 1 | |a Longo, Michele |e verfasserin |4 aut | |
| 700 | 1 | |a Beguinot, Francesco |e verfasserin |4 aut | |
| 700 | 1 | |a Ungaro, Paola |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Metabolism |d Orlando, Fla. : Elsevier, 1964 |g 87, Seite 70-79 |h Online-Ressource |w (DE-627)330080490 |w (DE-600)2049062-8 |w (DE-576)105536792 |x 1532-8600 |7 nnns |
| 773 | 1 | 8 | |g volume:87 |g pages:70-79 |
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2018 |
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10.1016/j.metabol.2018.06.001 doi (DE-627)ELV000682500 (ELSEVIER)S0026-0495(18)30135-5 DE-627 ger DE-627 rda eng 610 DE-600 35.70 bkl Vastolo, Viviana verfasserin aut High-fat diet unveils an enhancer element at the 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes Nettore, Immacolata Cristina verfasserin aut Ciccarelli, Marco verfasserin aut Albano, Luigi verfasserin aut Raciti, Gregory Alexander verfasserin aut Longo, Michele verfasserin aut Beguinot, Francesco verfasserin aut Ungaro, Paola verfasserin aut Enthalten in Metabolism Orlando, Fla. : Elsevier, 1964 87, Seite 70-79 Online-Ressource (DE-627)330080490 (DE-600)2049062-8 (DE-576)105536792 1532-8600 nnns volume:87 pages:70-79 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 35.70 Biochemie: Allgemeines AR 87 70-79 |
| spelling |
10.1016/j.metabol.2018.06.001 doi (DE-627)ELV000682500 (ELSEVIER)S0026-0495(18)30135-5 DE-627 ger DE-627 rda eng 610 DE-600 35.70 bkl Vastolo, Viviana verfasserin aut High-fat diet unveils an enhancer element at the 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes Nettore, Immacolata Cristina verfasserin aut Ciccarelli, Marco verfasserin aut Albano, Luigi verfasserin aut Raciti, Gregory Alexander verfasserin aut Longo, Michele verfasserin aut Beguinot, Francesco verfasserin aut Ungaro, Paola verfasserin aut Enthalten in Metabolism Orlando, Fla. : Elsevier, 1964 87, Seite 70-79 Online-Ressource (DE-627)330080490 (DE-600)2049062-8 (DE-576)105536792 1532-8600 nnns volume:87 pages:70-79 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 35.70 Biochemie: Allgemeines AR 87 70-79 |
| allfields_unstemmed |
10.1016/j.metabol.2018.06.001 doi (DE-627)ELV000682500 (ELSEVIER)S0026-0495(18)30135-5 DE-627 ger DE-627 rda eng 610 DE-600 35.70 bkl Vastolo, Viviana verfasserin aut High-fat diet unveils an enhancer element at the 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes Nettore, Immacolata Cristina verfasserin aut Ciccarelli, Marco verfasserin aut Albano, Luigi verfasserin aut Raciti, Gregory Alexander verfasserin aut Longo, Michele verfasserin aut Beguinot, Francesco verfasserin aut Ungaro, Paola verfasserin aut Enthalten in Metabolism Orlando, Fla. : Elsevier, 1964 87, Seite 70-79 Online-Ressource (DE-627)330080490 (DE-600)2049062-8 (DE-576)105536792 1532-8600 nnns volume:87 pages:70-79 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 35.70 Biochemie: Allgemeines AR 87 70-79 |
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10.1016/j.metabol.2018.06.001 doi (DE-627)ELV000682500 (ELSEVIER)S0026-0495(18)30135-5 DE-627 ger DE-627 rda eng 610 DE-600 35.70 bkl Vastolo, Viviana verfasserin aut High-fat diet unveils an enhancer element at the 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes Nettore, Immacolata Cristina verfasserin aut Ciccarelli, Marco verfasserin aut Albano, Luigi verfasserin aut Raciti, Gregory Alexander verfasserin aut Longo, Michele verfasserin aut Beguinot, Francesco verfasserin aut Ungaro, Paola verfasserin aut Enthalten in Metabolism Orlando, Fla. : Elsevier, 1964 87, Seite 70-79 Online-Ressource (DE-627)330080490 (DE-600)2049062-8 (DE-576)105536792 1532-8600 nnns volume:87 pages:70-79 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 35.70 Biochemie: Allgemeines AR 87 70-79 |
| allfieldsSound |
10.1016/j.metabol.2018.06.001 doi (DE-627)ELV000682500 (ELSEVIER)S0026-0495(18)30135-5 DE-627 ger DE-627 rda eng 610 DE-600 35.70 bkl Vastolo, Viviana verfasserin aut High-fat diet unveils an enhancer element at the 2018 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes Nettore, Immacolata Cristina verfasserin aut Ciccarelli, Marco verfasserin aut Albano, Luigi verfasserin aut Raciti, Gregory Alexander verfasserin aut Longo, Michele verfasserin aut Beguinot, Francesco verfasserin aut Ungaro, Paola verfasserin aut Enthalten in Metabolism Orlando, Fla. : Elsevier, 1964 87, Seite 70-79 Online-Ressource (DE-627)330080490 (DE-600)2049062-8 (DE-576)105536792 1532-8600 nnns volume:87 pages:70-79 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 35.70 Biochemie: Allgemeines AR 87 70-79 |
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Enthalten in Metabolism 87, Seite 70-79 volume:87 pages:70-79 |
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Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes |
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Vastolo, Viviana @@aut@@ Nettore, Immacolata Cristina @@aut@@ Ciccarelli, Marco @@aut@@ Albano, Luigi @@aut@@ Raciti, Gregory Alexander @@aut@@ Longo, Michele @@aut@@ Beguinot, Francesco @@aut@@ Ungaro, Paola @@aut@@ |
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2018-01-01T00:00:00Z |
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Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. 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Vastolo, Viviana |
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Vastolo, Viviana ddc 610 bkl 35.70 misc Chromatin remodelling misc Enhancer misc Metabolic memory misc Type 2 diabetes High-fat diet unveils an enhancer element at the |
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610 DE-600 35.70 bkl High-fat diet unveils an enhancer element at the Chromatin remodelling Enhancer Metabolic memory Type 2 diabetes |
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ddc 610 bkl 35.70 misc Chromatin remodelling misc Enhancer misc Metabolic memory misc Type 2 diabetes |
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Vastolo, Viviana Nettore, Immacolata Cristina Ciccarelli, Marco Albano, Luigi Raciti, Gregory Alexander Longo, Michele Beguinot, Francesco Ungaro, Paola |
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high-fat diet unveils an enhancer element at the |
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High-fat diet unveils an enhancer element at the |
| abstract |
Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. |
| abstractGer |
Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. |
| abstract_unstemmed |
Background: The impact of nutrition on the evolution towards type 2 diabetes has recently received increasing attention because of the effect on chromatin structure and gene expression.Purpose: Evaluate the effect of high-fat diet on chromatin remodelling and expression of Ped/Pea-15, a gene commonly overexpressed in individuals at risk of type 2 diabetes.Methods: We used mouse and cell models to investigate Ped/Pea-15 transcriptional regulation by high-fat diet and glucose, respectively. Chromatin structure and histone modification marks were assessed by Micrococcal Nuclease Protection and Chromatin Immunoprecipitation assays.Results: Sixteen-week exposure of C57BL/6J mice to a high-fat diet impaired glucose tolerance and enhanced Ped/Pea-15 expression in their skeletal muscle tissue. This effect was associated with increased chromatin accessibility at specific regulatory sites at the Ped/Pea-15 gene. In particular, the region at −1900 to −1300 bp from Ped/Pea-15 transcription start site was revealed to feature enhancer activity as demonstrated by its function in the luciferase assay, increased p300 recruitment and H3K4me1 and H3K27Ac levels, all marks of functionally active enhancers. Returning mice to a standard chow diet was accompanied by rapid loss of acetylation of K27 on histone H3 and p300 recruitment at Ped/Pea-15. In contrast, the increased H3K4me1, which accompanied the high-fat diet exposure, remained stable. Incubation of muscle cells in culture medium supplemented with 25 mM glucose (HG) increased Ped/Pea-15 mRNA expression and H3K4me1 at the enhancer region. These effects became measurable upon 72 h of exposure to the HG medium and were not rescued upon returning the cells to the 5 mM glucose-containing medium. Interestingly, after 25 mM and sequential 5 mM glucose treatments, re-exposure of the same cells to HG medium further enhanced Ped/Pea-15 expression and increased H3K4me1 above the levels induced by the initial HG challenge already upon 24 h.Conclusion: Transient exposure to HFD or HG unveiled the presence of an enhancer element at the Ped/Pea-15 gene. Epigenetic changes imposed at this region by diets, which impair glucose tolerance generate metabolic memory of the nutritional injury and leave Ped/Pea-15 induction in a poised state. |
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| score |
7.401991 |