Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion
Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthe...
Ausführliche Beschreibung
Autor*in: |
Fernandes Gregnani, Marcos [verfasserIn] Budu, Alexandre [verfasserIn] Batista, Rogério Oliveira [verfasserIn] Ornellas, Fábio Henrique [verfasserIn] Estrela, Gabriel Rufino [verfasserIn] Arruda, Adriano Cleis [verfasserIn] Freitas Lima, Leandro Ceotto [verfasserIn] Kremer, Jean Lucas [verfasserIn] Favaroni Mendes, Lys Angela [verfasserIn] Casarini, Dulce Elena [verfasserIn] Lotfi, Claudimara Ferini Pacicco [verfasserIn] Oyama, Lila Missae [verfasserIn] Bader, Michael [verfasserIn] Araújo, Ronaldo Carvalho [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2023 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Molecular and cellular endocrinology - Amsterdam [u.a.] : Elsevier Science, 1974, 579 |
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Übergeordnetes Werk: |
volume:579 |
DOI / URN: |
10.1016/j.mce.2023.112085 |
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Katalog-ID: |
ELV066087481 |
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245 | 1 | 0 | |a Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion |
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520 | |a Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. | ||
650 | 4 | |a Catecholamines | |
650 | 4 | |a Kinin receptors | |
650 | 4 | |a Physical exercise | |
650 | 4 | |a Glucose homeostasis | |
700 | 1 | |a Budu, Alexandre |e verfasserin |4 aut | |
700 | 1 | |a Batista, Rogério Oliveira |e verfasserin |4 aut | |
700 | 1 | |a Ornellas, Fábio Henrique |e verfasserin |4 aut | |
700 | 1 | |a Estrela, Gabriel Rufino |e verfasserin |0 (orcid)0000-0003-2858-5111 |4 aut | |
700 | 1 | |a Arruda, Adriano Cleis |e verfasserin |4 aut | |
700 | 1 | |a Freitas Lima, Leandro Ceotto |e verfasserin |4 aut | |
700 | 1 | |a Kremer, Jean Lucas |e verfasserin |0 (orcid)0000-0002-0053-8500 |4 aut | |
700 | 1 | |a Favaroni Mendes, Lys Angela |e verfasserin |0 (orcid)0000-0002-4388-9087 |4 aut | |
700 | 1 | |a Casarini, Dulce Elena |e verfasserin |4 aut | |
700 | 1 | |a Lotfi, Claudimara Ferini Pacicco |e verfasserin |4 aut | |
700 | 1 | |a Oyama, Lila Missae |e verfasserin |0 (orcid)0000-0002-7078-6526 |4 aut | |
700 | 1 | |a Bader, Michael |e verfasserin |0 (orcid)0000-0003-4780-4164 |4 aut | |
700 | 1 | |a Araújo, Ronaldo Carvalho |e verfasserin |4 aut | |
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allfields |
10.1016/j.mce.2023.112085 doi (DE-627)ELV066087481 (ELSEVIER)S0303-7207(23)00236-8 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Fernandes Gregnani, Marcos verfasserin aut Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. Catecholamines Kinin receptors Physical exercise Glucose homeostasis Budu, Alexandre verfasserin aut Batista, Rogério Oliveira verfasserin aut Ornellas, Fábio Henrique verfasserin aut Estrela, Gabriel Rufino verfasserin (orcid)0000-0003-2858-5111 aut Arruda, Adriano Cleis verfasserin aut Freitas Lima, Leandro Ceotto verfasserin aut Kremer, Jean Lucas verfasserin (orcid)0000-0002-0053-8500 aut Favaroni Mendes, Lys Angela verfasserin (orcid)0000-0002-4388-9087 aut Casarini, Dulce Elena verfasserin aut Lotfi, Claudimara Ferini Pacicco verfasserin aut Oyama, Lila Missae verfasserin (orcid)0000-0002-7078-6526 aut Bader, Michael verfasserin (orcid)0000-0003-4780-4164 aut Araújo, Ronaldo Carvalho verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 579 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:579 GBV_USEFLAG_U GBV_ELV SYSFLAG_U 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.89 Endokrinologie VZ AR 579 |
spelling |
10.1016/j.mce.2023.112085 doi (DE-627)ELV066087481 (ELSEVIER)S0303-7207(23)00236-8 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Fernandes Gregnani, Marcos verfasserin aut Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. Catecholamines Kinin receptors Physical exercise Glucose homeostasis Budu, Alexandre verfasserin aut Batista, Rogério Oliveira verfasserin aut Ornellas, Fábio Henrique verfasserin aut Estrela, Gabriel Rufino verfasserin (orcid)0000-0003-2858-5111 aut Arruda, Adriano Cleis verfasserin aut Freitas Lima, Leandro Ceotto verfasserin aut Kremer, Jean Lucas verfasserin (orcid)0000-0002-0053-8500 aut Favaroni Mendes, Lys Angela verfasserin (orcid)0000-0002-4388-9087 aut Casarini, Dulce Elena verfasserin aut Lotfi, Claudimara Ferini Pacicco verfasserin aut Oyama, Lila Missae verfasserin (orcid)0000-0002-7078-6526 aut Bader, Michael verfasserin (orcid)0000-0003-4780-4164 aut Araújo, Ronaldo Carvalho verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 579 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:579 GBV_USEFLAG_U GBV_ELV SYSFLAG_U 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.89 Endokrinologie VZ AR 579 |
allfields_unstemmed |
10.1016/j.mce.2023.112085 doi (DE-627)ELV066087481 (ELSEVIER)S0303-7207(23)00236-8 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Fernandes Gregnani, Marcos verfasserin aut Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. Catecholamines Kinin receptors Physical exercise Glucose homeostasis Budu, Alexandre verfasserin aut Batista, Rogério Oliveira verfasserin aut Ornellas, Fábio Henrique verfasserin aut Estrela, Gabriel Rufino verfasserin (orcid)0000-0003-2858-5111 aut Arruda, Adriano Cleis verfasserin aut Freitas Lima, Leandro Ceotto verfasserin aut Kremer, Jean Lucas verfasserin (orcid)0000-0002-0053-8500 aut Favaroni Mendes, Lys Angela verfasserin (orcid)0000-0002-4388-9087 aut Casarini, Dulce Elena verfasserin aut Lotfi, Claudimara Ferini Pacicco verfasserin aut Oyama, Lila Missae verfasserin (orcid)0000-0002-7078-6526 aut Bader, Michael verfasserin (orcid)0000-0003-4780-4164 aut Araújo, Ronaldo Carvalho verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 579 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:579 GBV_USEFLAG_U GBV_ELV SYSFLAG_U 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.89 Endokrinologie VZ AR 579 |
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10.1016/j.mce.2023.112085 doi (DE-627)ELV066087481 (ELSEVIER)S0303-7207(23)00236-8 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Fernandes Gregnani, Marcos verfasserin aut Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. Catecholamines Kinin receptors Physical exercise Glucose homeostasis Budu, Alexandre verfasserin aut Batista, Rogério Oliveira verfasserin aut Ornellas, Fábio Henrique verfasserin aut Estrela, Gabriel Rufino verfasserin (orcid)0000-0003-2858-5111 aut Arruda, Adriano Cleis verfasserin aut Freitas Lima, Leandro Ceotto verfasserin aut Kremer, Jean Lucas verfasserin (orcid)0000-0002-0053-8500 aut Favaroni Mendes, Lys Angela verfasserin (orcid)0000-0002-4388-9087 aut Casarini, Dulce Elena verfasserin aut Lotfi, Claudimara Ferini Pacicco verfasserin aut Oyama, Lila Missae verfasserin (orcid)0000-0002-7078-6526 aut Bader, Michael verfasserin (orcid)0000-0003-4780-4164 aut Araújo, Ronaldo Carvalho verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 579 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:579 GBV_USEFLAG_U GBV_ELV SYSFLAG_U 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.89 Endokrinologie VZ AR 579 |
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10.1016/j.mce.2023.112085 doi (DE-627)ELV066087481 (ELSEVIER)S0303-7207(23)00236-8 DE-627 ger DE-627 rda eng 610 570 VZ 44.89 bkl Fernandes Gregnani, Marcos verfasserin aut Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. Catecholamines Kinin receptors Physical exercise Glucose homeostasis Budu, Alexandre verfasserin aut Batista, Rogério Oliveira verfasserin aut Ornellas, Fábio Henrique verfasserin aut Estrela, Gabriel Rufino verfasserin (orcid)0000-0003-2858-5111 aut Arruda, Adriano Cleis verfasserin aut Freitas Lima, Leandro Ceotto verfasserin aut Kremer, Jean Lucas verfasserin (orcid)0000-0002-0053-8500 aut Favaroni Mendes, Lys Angela verfasserin (orcid)0000-0002-4388-9087 aut Casarini, Dulce Elena verfasserin aut Lotfi, Claudimara Ferini Pacicco verfasserin aut Oyama, Lila Missae verfasserin (orcid)0000-0002-7078-6526 aut Bader, Michael verfasserin (orcid)0000-0003-4780-4164 aut Araújo, Ronaldo Carvalho verfasserin aut Enthalten in Molecular and cellular endocrinology Amsterdam [u.a.] : Elsevier Science, 1974 579 Online-Ressource (DE-627)306661217 (DE-600)1500651-7 (DE-576)081986807 1872-8057 nnns volume:579 GBV_USEFLAG_U GBV_ELV SYSFLAG_U 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_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.89 Endokrinologie VZ AR 579 |
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Enthalten in Molecular and cellular endocrinology 579 volume:579 |
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Enthalten in Molecular and cellular endocrinology 579 volume:579 |
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Catecholamines Kinin receptors Physical exercise Glucose homeostasis |
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container_title |
Molecular and cellular endocrinology |
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Fernandes Gregnani, Marcos @@aut@@ Budu, Alexandre @@aut@@ Batista, Rogério Oliveira @@aut@@ Ornellas, Fábio Henrique @@aut@@ Estrela, Gabriel Rufino @@aut@@ Arruda, Adriano Cleis @@aut@@ Freitas Lima, Leandro Ceotto @@aut@@ Kremer, Jean Lucas @@aut@@ Favaroni Mendes, Lys Angela @@aut@@ Casarini, Dulce Elena @@aut@@ Lotfi, Claudimara Ferini Pacicco @@aut@@ Oyama, Lila Missae @@aut@@ Bader, Michael @@aut@@ Araújo, Ronaldo Carvalho @@aut@@ |
publishDateDaySort_date |
2023-01-01T00:00:00Z |
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3610 |
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ELV066087481 |
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Fernandes Gregnani, Marcos |
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610 570 VZ 44.89 bkl Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion Catecholamines Kinin receptors Physical exercise Glucose homeostasis |
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Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion |
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Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion |
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Fernandes Gregnani, Marcos Budu, Alexandre Batista, Rogério Oliveira Ornellas, Fábio Henrique Estrela, Gabriel Rufino Arruda, Adriano Cleis Freitas Lima, Leandro Ceotto Kremer, Jean Lucas Favaroni Mendes, Lys Angela Casarini, Dulce Elena Lotfi, Claudimara Ferini Pacicco Oyama, Lila Missae Bader, Michael Araújo, Ronaldo Carvalho |
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kinin b1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion |
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Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion |
abstract |
Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. |
abstractGer |
Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. |
abstract_unstemmed |
Our group has shown in several papers that kinin B1 receptor (B1R) is involved in metabolic adaptations, mediating glucose homeostasis and interfering in leptin and insulin signaling. Since catecholamines are involved with metabolism management, we sought to evaluate B1R role in catecholamine synthesis/secretion. Using B1R global knockout mice, we observed increased basal epinephrine content, accompanied by decreased hepatic glycogen content and increased glucosuria. When these mice were challenged with maximal intensity exercise, they showed decreased epinephrine and norepinephrine response, accompanied by disturbed glycemic responses to effort and poor performance. This phenotype was related to alterations in adrenal catecholamine synthesis: increased basal epinephrine concentration and reduced norepinephrine content in response to exercise, as well decreased gene expression and protein content of tyrosine hydroxylase and decreased gene expression of dopamine beta hydroxylase and kinin B2 receptor. We conclude that the global absence of B1R impairs catecholamine synthesis, interfering with glucose metabolism at rest and during maximal exercise. |
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title_short |
Kinin B1 receptor modulates glucose homeostasis and physical exercise capacity by altering adrenal catecholamine synthesis and secretion |
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Budu, Alexandre Batista, Rogério Oliveira Ornellas, Fábio Henrique Estrela, Gabriel Rufino Arruda, Adriano Cleis Freitas Lima, Leandro Ceotto Kremer, Jean Lucas Favaroni Mendes, Lys Angela Casarini, Dulce Elena Lotfi, Claudimara Ferini Pacicco Oyama, Lila Missae Bader, Michael Araújo, Ronaldo Carvalho |
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7.4001293 |