Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons

<p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Pinelis Vsevolod G [verfasserIn] Persiyantseva Nadezhda A [verfasserIn] Senilova Yana E [verfasserIn] Storozhevykh Tatiana P [verfasserIn] Pomytkin Igor A [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Übergeordnetes Werk:	In: BMC Neuroscience - BMC, 2003, 8(2007), 1, p 84
Übergeordnetes Werk:	volume:8 ; year:2007 ; number:1, p 84

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2202-8-84

Katalog-ID:	DOAJ065597990

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allfields	10.1186/1471-2202-8-84 doi (DE-627)DOAJ065597990 (DE-599)DOAJb47c4e02f849468cbd5aaf183c5accd7 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Pinelis Vsevolod G verfasserin aut Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Persiyantseva Nadezhda A verfasserin aut Senilova Yana E verfasserin aut Storozhevykh Tatiana P verfasserin aut Pomytkin Igor A verfasserin aut In BMC Neuroscience BMC, 2003 8(2007), 1, p 84 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:8 year:2007 number:1, p 84 https://doi.org/10.1186/1471-2202-8-84 kostenfrei https://doaj.org/article/b47c4e02f849468cbd5aaf183c5accd7 kostenfrei http://www.biomedcentral.com/1471-2202/8/84 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1, p 84
spelling	10.1186/1471-2202-8-84 doi (DE-627)DOAJ065597990 (DE-599)DOAJb47c4e02f849468cbd5aaf183c5accd7 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Pinelis Vsevolod G verfasserin aut Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Persiyantseva Nadezhda A verfasserin aut Senilova Yana E verfasserin aut Storozhevykh Tatiana P verfasserin aut Pomytkin Igor A verfasserin aut In BMC Neuroscience BMC, 2003 8(2007), 1, p 84 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:8 year:2007 number:1, p 84 https://doi.org/10.1186/1471-2202-8-84 kostenfrei https://doaj.org/article/b47c4e02f849468cbd5aaf183c5accd7 kostenfrei http://www.biomedcentral.com/1471-2202/8/84 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1, p 84
allfields_unstemmed	10.1186/1471-2202-8-84 doi (DE-627)DOAJ065597990 (DE-599)DOAJb47c4e02f849468cbd5aaf183c5accd7 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Pinelis Vsevolod G verfasserin aut Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Persiyantseva Nadezhda A verfasserin aut Senilova Yana E verfasserin aut Storozhevykh Tatiana P verfasserin aut Pomytkin Igor A verfasserin aut In BMC Neuroscience BMC, 2003 8(2007), 1, p 84 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:8 year:2007 number:1, p 84 https://doi.org/10.1186/1471-2202-8-84 kostenfrei https://doaj.org/article/b47c4e02f849468cbd5aaf183c5accd7 kostenfrei http://www.biomedcentral.com/1471-2202/8/84 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1, p 84
allfieldsGer	10.1186/1471-2202-8-84 doi (DE-627)DOAJ065597990 (DE-599)DOAJb47c4e02f849468cbd5aaf183c5accd7 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Pinelis Vsevolod G verfasserin aut Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Persiyantseva Nadezhda A verfasserin aut Senilova Yana E verfasserin aut Storozhevykh Tatiana P verfasserin aut Pomytkin Igor A verfasserin aut In BMC Neuroscience BMC, 2003 8(2007), 1, p 84 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:8 year:2007 number:1, p 84 https://doi.org/10.1186/1471-2202-8-84 kostenfrei https://doaj.org/article/b47c4e02f849468cbd5aaf183c5accd7 kostenfrei http://www.biomedcentral.com/1471-2202/8/84 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1, p 84
allfieldsSound	10.1186/1471-2202-8-84 doi (DE-627)DOAJ065597990 (DE-599)DOAJb47c4e02f849468cbd5aaf183c5accd7 DE-627 ger DE-627 rakwb eng RC321-571 QP351-495 Pinelis Vsevolod G verfasserin aut Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p< Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology Persiyantseva Nadezhda A verfasserin aut Senilova Yana E verfasserin aut Storozhevykh Tatiana P verfasserin aut Pomytkin Igor A verfasserin aut In BMC Neuroscience BMC, 2003 8(2007), 1, p 84 (DE-627)326643648 (DE-600)2041344-0 14712202 nnns volume:8 year:2007 number:1, p 84 https://doi.org/10.1186/1471-2202-8-84 kostenfrei https://doaj.org/article/b47c4e02f849468cbd5aaf183c5accd7 kostenfrei http://www.biomedcentral.com/1471-2202/8/84 kostenfrei https://doaj.org/toc/1471-2202 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2007 1, p 84
language	English
source	In BMC Neuroscience 8(2007), 1, p 84 volume:8 year:2007 number:1, p 84
sourceStr	In BMC Neuroscience 8(2007), 1, p 84 volume:8 year:2007 number:1, p 84
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Neurosciences. Biological psychiatry. Neuropsychiatry Neurophysiology and neuropsychology
isfreeaccess_bool	true
container_title	BMC Neuroscience
authorswithroles_txt_mv	Pinelis Vsevolod G @@aut@@ Persiyantseva Nadezhda A @@aut@@ Senilova Yana E @@aut@@ Storozhevykh Tatiana P @@aut@@ Pomytkin Igor A @@aut@@
publishDateDaySort_date	2007-01-01T00:00:00Z
hierarchy_top_id	326643648
id	DOAJ065597990
language_de	englisch
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The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. 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callnumber-first	R - Medicine
author	Pinelis Vsevolod G
spellingShingle	Pinelis Vsevolod G misc RC321-571 misc QP351-495 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurophysiology and neuropsychology Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
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topic_title	RC321-571 QP351-495 Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
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topic_unstemmed	misc RC321-571 misc QP351-495 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurophysiology and neuropsychology
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title	Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
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title_full	Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
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author_browse	Pinelis Vsevolod G Persiyantseva Nadezhda A Senilova Yana E Storozhevykh Tatiana P Pomytkin Igor A
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title_sort	mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
callnumber	RC321-571
title_auth	Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
abstract	<p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<Accumulated evidence suggests that hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p<
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title_short	Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
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The role of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neuronal insulin receptor activation and the origin of insulin-induced H<sub<2</sub<O<sub<2 </sub<in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in insulin receptor autophosphorylation in neurons.</p< <p<Results</p< <p<Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in H<sub<2</sub<O<sub<2 </sub<release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a H<sub<2</sub<O<sub<2 </sub<scavenger, inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated H<sub<2</sub<O<sub<2 </sub<production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated H<sub<2</sub<O<sub<2 </sub<release from neurons and insulin-stimulated autophosphorylation of insulin receptor. Dicholine salt of succinic acid, a respiratory substrate, significantly enhanced the effect of suboptimal insulin concentration on the insulin receptor autophosphorylation in CGN.</p< <p<Conclusion</p< <p<Results of the present study suggest that insulin-induced H<sub<2</sub<O<sub<2 </sub<is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated H<sub<2</sub<O<sub<2 </sub<production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.</p<</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neurosciences. Biological psychiatry. 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Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons

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