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

Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of...
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Autor*in:	Storozhevykh, Tatiana P [verfasserIn] Senilova, Yana E Persiyantseva, Nadezhda A Pinelis, Vsevolod G Pomytkin, Igor A

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Schlagwörter:	Insulin Receptor Succinic Acid Mitochondrial Respiratory Chain H2O2 Production H2O2 Generation

Anmerkung:	© Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: BMC neuroscience - London : BioMed Central, 2000, 8(2007), 1 vom: 08. Okt.
Übergeordnetes Werk:	volume:8 ; year:2007 ; number:1 ; day:08 ; month:10

Links:	Volltext

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

Katalog-ID:	SPR027225704

Internformat


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100	1		\|a Storozhevykh, Tatiana P \|e verfasserin \|4 aut
245	1	0	\|a 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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520			\|a Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons.
650		4	\|a Insulin Receptor \|7 (dpeaa)DE-He213
650		4	\|a Succinic Acid \|7 (dpeaa)DE-He213
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700	1		\|a Senilova, Yana E \|4 aut
700	1		\|a Persiyantseva, Nadezhda A \|4 aut
700	1		\|a Pinelis, Vsevolod G \|4 aut
700	1		\|a Pomytkin, Igor A \|4 aut
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951			\|a AR
952			\|d 8 \|j 2007 \|e 1 \|b 08 \|c 10

Indexfelder

author_variant	t p s tp tps y e s ye yes n a p na nap v g p vg vgp i a p ia iap
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publishDate	2007
allfields	10.1186/1471-2202-8-84 doi (DE-627)SPR027225704 (SPR)1471-2202-8-84-e DE-627 ger DE-627 rakwb eng Storozhevykh, Tatiana P 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 © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. Insulin Receptor (dpeaa)DE-He213 Succinic Acid (dpeaa)DE-He213 Mitochondrial Respiratory Chain (dpeaa)DE-He213 H2O2 Production (dpeaa)DE-He213 H2O2 Generation (dpeaa)DE-He213 Senilova, Yana E aut Persiyantseva, Nadezhda A aut Pinelis, Vsevolod G aut Pomytkin, Igor A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 8(2007), 1 vom: 08. Okt. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:8 year:2007 number:1 day:08 month:10 https://dx.doi.org/10.1186/1471-2202-8-84 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_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 08 10
spelling	10.1186/1471-2202-8-84 doi (DE-627)SPR027225704 (SPR)1471-2202-8-84-e DE-627 ger DE-627 rakwb eng Storozhevykh, Tatiana P 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 © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. Insulin Receptor (dpeaa)DE-He213 Succinic Acid (dpeaa)DE-He213 Mitochondrial Respiratory Chain (dpeaa)DE-He213 H2O2 Production (dpeaa)DE-He213 H2O2 Generation (dpeaa)DE-He213 Senilova, Yana E aut Persiyantseva, Nadezhda A aut Pinelis, Vsevolod G aut Pomytkin, Igor A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 8(2007), 1 vom: 08. Okt. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:8 year:2007 number:1 day:08 month:10 https://dx.doi.org/10.1186/1471-2202-8-84 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_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 08 10
allfields_unstemmed	10.1186/1471-2202-8-84 doi (DE-627)SPR027225704 (SPR)1471-2202-8-84-e DE-627 ger DE-627 rakwb eng Storozhevykh, Tatiana P 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 © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. Insulin Receptor (dpeaa)DE-He213 Succinic Acid (dpeaa)DE-He213 Mitochondrial Respiratory Chain (dpeaa)DE-He213 H2O2 Production (dpeaa)DE-He213 H2O2 Generation (dpeaa)DE-He213 Senilova, Yana E aut Persiyantseva, Nadezhda A aut Pinelis, Vsevolod G aut Pomytkin, Igor A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 8(2007), 1 vom: 08. Okt. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:8 year:2007 number:1 day:08 month:10 https://dx.doi.org/10.1186/1471-2202-8-84 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_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 08 10
allfieldsGer	10.1186/1471-2202-8-84 doi (DE-627)SPR027225704 (SPR)1471-2202-8-84-e DE-627 ger DE-627 rakwb eng Storozhevykh, Tatiana P 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 © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. Insulin Receptor (dpeaa)DE-He213 Succinic Acid (dpeaa)DE-He213 Mitochondrial Respiratory Chain (dpeaa)DE-He213 H2O2 Production (dpeaa)DE-He213 H2O2 Generation (dpeaa)DE-He213 Senilova, Yana E aut Persiyantseva, Nadezhda A aut Pinelis, Vsevolod G aut Pomytkin, Igor A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 8(2007), 1 vom: 08. Okt. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:8 year:2007 number:1 day:08 month:10 https://dx.doi.org/10.1186/1471-2202-8-84 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_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 08 10
allfieldsSound	10.1186/1471-2202-8-84 doi (DE-627)SPR027225704 (SPR)1471-2202-8-84-e DE-627 ger DE-627 rakwb eng Storozhevykh, Tatiana P 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 © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. Insulin Receptor (dpeaa)DE-He213 Succinic Acid (dpeaa)DE-He213 Mitochondrial Respiratory Chain (dpeaa)DE-He213 H2O2 Production (dpeaa)DE-He213 H2O2 Generation (dpeaa)DE-He213 Senilova, Yana E aut Persiyantseva, Nadezhda A aut Pinelis, Vsevolod G aut Pomytkin, Igor A aut Enthalten in BMC neuroscience London : BioMed Central, 2000 8(2007), 1 vom: 08. Okt. (DE-627)326643648 (DE-600)2041344-0 1471-2202 nnns volume:8 year:2007 number:1 day:08 month:10 https://dx.doi.org/10.1186/1471-2202-8-84 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_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 08 10
language	English
source	Enthalten in BMC neuroscience 8(2007), 1 vom: 08. Okt. volume:8 year:2007 number:1 day:08 month:10
sourceStr	Enthalten in BMC neuroscience 8(2007), 1 vom: 08. Okt. volume:8 year:2007 number:1 day:08 month:10
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Insulin Receptor Succinic Acid Mitochondrial Respiratory Chain H2O2 Production H2O2 Generation
isfreeaccess_bool	false
container_title	BMC neuroscience
authorswithroles_txt_mv	Storozhevykh, Tatiana P @@aut@@ Senilova, Yana E @@aut@@ Persiyantseva, Nadezhda A @@aut@@ Pinelis, Vsevolod G @@aut@@ Pomytkin, Igor A @@aut@@
publishDateDaySort_date	2007-10-08T00:00:00Z
hierarchy_top_id	326643648
id	SPR027225704
language_de	englisch
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. 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author	Storozhevykh, Tatiana P
spellingShingle	Storozhevykh, Tatiana P misc Insulin Receptor misc Succinic Acid misc Mitochondrial Respiratory Chain misc H2O2 Production misc H2O2 Generation 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	Mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons Insulin Receptor (dpeaa)DE-He213 Succinic Acid (dpeaa)DE-He213 Mitochondrial Respiratory Chain (dpeaa)DE-He213 H2O2 Production (dpeaa)DE-He213 H2O2 Generation (dpeaa)DE-He213
topic	misc Insulin Receptor misc Succinic Acid misc Mitochondrial Respiratory Chain misc H2O2 Production misc H2O2 Generation
topic_unstemmed	misc Insulin Receptor misc Succinic Acid misc Mitochondrial Respiratory Chain misc H2O2 Production misc H2O2 Generation
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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
author_sort	Storozhevykh, Tatiana P
journal	BMC neuroscience
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author_browse	Storozhevykh, Tatiana P Senilova, Yana E Persiyantseva, Nadezhda A Pinelis, Vsevolod G Pomytkin, Igor A
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author-letter	Storozhevykh, Tatiana P
doi_str_mv	10.1186/1471-2202-8-84
title_sort	mitochondrial respiratory chain is involved in insulin-stimulated hydrogen peroxide production and plays an integral role in insulin receptor autophosphorylation in neurons
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	Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. The mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in the insulin receptor autophosphorylation in neurons. © Storozhevykh et al.; licensee BioMed Central Ltd. 2007. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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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
url	https://dx.doi.org/10.1186/1471-2202-8-84
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author2	Senilova, Yana E Persiyantseva, Nadezhda A Pinelis, Vsevolod G Pomytkin, Igor A
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up_date	2024-07-04T00:58:24.846Z
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Accumulated evidence suggests that hydrogen peroxide ($ H_{2} %$ O_{2} $) generated in cells during insulin stimulation plays an integral role in insulin receptor signal transduction. The role of insulin-induced $ H_{2} %$ O_{2} $ in neuronal insulin receptor activation and the origin of insulin-induced $ H_{2} %$ O_{2} $ in neurons remain unclear. The aim of the present study is to test the following hypotheses (1) whether insulin-induced $ H_{2} %$ O_{2} $ is required for insulin receptor autophosphorylation in neurons, and (2) whether mitochondrial respiratory chain is involved in insulin-stimulated $ H_{2} %$ O_{2} $ production, thus playing an integral role in insulin receptor autophosphorylation in neurons. Results Insulin stimulation elicited rapid insulin receptor autophosphorylation accompanied by an increase in $ H_{2} %$ O_{2} $ release from cultured cerebellar granule neurons (CGN). N-acetylcysteine (NAC), a $ H_{2} %$ O_{2} $ scavenger, inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ release and insulin-stimulated autophosphorylation of insulin receptor. Inhibitors of respiratory chain-mediated $ H_{2} %$ O_{2} $ production, malonate and carbonyl cyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP), inhibited both insulin-stimulated $ H_{2} %$ O_{2} $ 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. Conclusion Results of the present study suggest that insulin-induced $ H_{2} %$ O_{2} $ is required for the enhancement of insulin receptor autophosphorylation in neurons. 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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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