Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte
- Autores
- Funk, Melania Iara; Conde, Melisa Ailén; Alza, Natalia Paola; Salvador, Gabriela Alejandra; Uranga, Romina Maria
- Año de publicación
- 2020
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Obesity is closely related to metabolic disturbances, with the latter majorly caused by adipose tissue dysfunction. Oxidative stress (OS), a major characteristic of dysfunctional adipose tissue, is considered a primary contributing factor to the etiopathogenesis of obesity and associated comorbidities. However, the biochemical mechanisms by which OS alters adipocyte biology still require to be fully uncovered. We have previously demonstrated that menadione, a synthetic vitamer of vitamin K known to generate intracellular oxygen species, impairs adipogenesis by inhibiting the PI3K/Akt pathway. Our goal in this work was to study the effect of menadione-induced OS on mature adipocytes. For this purpose, differentiated 3T3-L1 adipocytes were exposed to menadione (20 and 50 µM) for 5 h, and different biochemical parameters were assessed. The exposure to menadione resulted in increased cell oxidants (65% and 122% of control, for 20 and 50 µM, respectively). However, none of the concentrations of menadione tested had any significant effect on either cell viability or morphology. The expression of adipogenic markers was evaluated by Western blot. Menadione-induced OS caused a significant decrease in the expression of PPARγ (95% and 99%, for 20 and 50 μM menadione, respectively), FAS (70% and 88%, for 20 and 50 μM menadione, respectively), C/EBPα (75% and 93%, for 20 and 50 μM menadione, respectively), and FABP4 (30% for 50 μM menadione). No changes were detected in intracellular triglyceride levels after the incubation in the presence of menadione. However, when the exposure to menadione-dependent OS was extended to 24 h, the intracellular triglyceride content was augmented by 53% and 68% upon the exposure to 20 and 50 μM menadione, respectively. At the same time, ACC (the ratelimiting enzyme in fatty acid synthesis) was activated (32% and 38% decreased phosphorylation, for 20 and 50 μM menadione, respectively). On the other hand, menadione-triggered OS also activated lipolysis (40% for 50 μM menadione). Together, our results show that OS acutely modulates both the expression and activity of different lipo/adipogenic proteins, activating fatty acids’ metabolic turnover, with enhanced lipolysis, which is overcome by fatty acid synthesis, resulting in an increased triglyceride content. Our next goal is the unraveling of the cellular signaling responsible for these metabolic changes observed.
Fil: Funk, Melania Iara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Conde, Melisa Ailén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Alza, Natalia Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
LVI Reunión Anual Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; XV Reunión Anual de Sociedad Argentina de Microbiología General
Virtual
Argentina
Sociedad Argentina de Investigación Bioquímica y Biología Molecular
Sociedad Argentina de Microbiología General - Materia
-
MENADIONE
ADIPOCYTE
OBESITY
OXIDATIVE STRESS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/188114
Ver los metadatos del registro completo
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Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyteFunk, Melania IaraConde, Melisa AilénAlza, Natalia PaolaSalvador, Gabriela AlejandraUranga, Romina MariaMENADIONEADIPOCYTEOBESITYOXIDATIVE STRESShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Obesity is closely related to metabolic disturbances, with the latter majorly caused by adipose tissue dysfunction. Oxidative stress (OS), a major characteristic of dysfunctional adipose tissue, is considered a primary contributing factor to the etiopathogenesis of obesity and associated comorbidities. However, the biochemical mechanisms by which OS alters adipocyte biology still require to be fully uncovered. We have previously demonstrated that menadione, a synthetic vitamer of vitamin K known to generate intracellular oxygen species, impairs adipogenesis by inhibiting the PI3K/Akt pathway. Our goal in this work was to study the effect of menadione-induced OS on mature adipocytes. For this purpose, differentiated 3T3-L1 adipocytes were exposed to menadione (20 and 50 µM) for 5 h, and different biochemical parameters were assessed. The exposure to menadione resulted in increased cell oxidants (65% and 122% of control, for 20 and 50 µM, respectively). However, none of the concentrations of menadione tested had any significant effect on either cell viability or morphology. The expression of adipogenic markers was evaluated by Western blot. Menadione-induced OS caused a significant decrease in the expression of PPARγ (95% and 99%, for 20 and 50 μM menadione, respectively), FAS (70% and 88%, for 20 and 50 μM menadione, respectively), C/EBPα (75% and 93%, for 20 and 50 μM menadione, respectively), and FABP4 (30% for 50 μM menadione). No changes were detected in intracellular triglyceride levels after the incubation in the presence of menadione. However, when the exposure to menadione-dependent OS was extended to 24 h, the intracellular triglyceride content was augmented by 53% and 68% upon the exposure to 20 and 50 μM menadione, respectively. At the same time, ACC (the ratelimiting enzyme in fatty acid synthesis) was activated (32% and 38% decreased phosphorylation, for 20 and 50 μM menadione, respectively). On the other hand, menadione-triggered OS also activated lipolysis (40% for 50 μM menadione). Together, our results show that OS acutely modulates both the expression and activity of different lipo/adipogenic proteins, activating fatty acids’ metabolic turnover, with enhanced lipolysis, which is overcome by fatty acid synthesis, resulting in an increased triglyceride content. Our next goal is the unraveling of the cellular signaling responsible for these metabolic changes observed.Fil: Funk, Melania Iara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Conde, Melisa Ailén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Alza, Natalia Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaLVI Reunión Anual Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; XV Reunión Anual de Sociedad Argentina de Microbiología GeneralVirtualArgentinaSociedad Argentina de Investigación Bioquímica y Biología MolecularSociedad Argentina de Microbiología GeneralTech Science Press2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/188114Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte; LVI Reunión Anual Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; XV Reunión Anual de Sociedad Argentina de Microbiología General; Virtual; Argentina; 2020; 44-440327-95451667-5746CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.techscience.com/biocell/v45nSuppl.1/42376Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:59:10Zoai:ri.conicet.gov.ar:11336/188114instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 09:59:10.574CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| title |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| spellingShingle |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte Funk, Melania Iara MENADIONE ADIPOCYTE OBESITY OXIDATIVE STRESS |
| title_short |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| title_full |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| title_fullStr |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| title_full_unstemmed |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| title_sort |
Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte |
| dc.creator.none.fl_str_mv |
Funk, Melania Iara Conde, Melisa Ailén Alza, Natalia Paola Salvador, Gabriela Alejandra Uranga, Romina Maria |
| author |
Funk, Melania Iara |
| author_facet |
Funk, Melania Iara Conde, Melisa Ailén Alza, Natalia Paola Salvador, Gabriela Alejandra Uranga, Romina Maria |
| author_role |
author |
| author2 |
Conde, Melisa Ailén Alza, Natalia Paola Salvador, Gabriela Alejandra Uranga, Romina Maria |
| author2_role |
author author author author |
| dc.subject.none.fl_str_mv |
MENADIONE ADIPOCYTE OBESITY OXIDATIVE STRESS |
| topic |
MENADIONE ADIPOCYTE OBESITY OXIDATIVE STRESS |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
Obesity is closely related to metabolic disturbances, with the latter majorly caused by adipose tissue dysfunction. Oxidative stress (OS), a major characteristic of dysfunctional adipose tissue, is considered a primary contributing factor to the etiopathogenesis of obesity and associated comorbidities. However, the biochemical mechanisms by which OS alters adipocyte biology still require to be fully uncovered. We have previously demonstrated that menadione, a synthetic vitamer of vitamin K known to generate intracellular oxygen species, impairs adipogenesis by inhibiting the PI3K/Akt pathway. Our goal in this work was to study the effect of menadione-induced OS on mature adipocytes. For this purpose, differentiated 3T3-L1 adipocytes were exposed to menadione (20 and 50 µM) for 5 h, and different biochemical parameters were assessed. The exposure to menadione resulted in increased cell oxidants (65% and 122% of control, for 20 and 50 µM, respectively). However, none of the concentrations of menadione tested had any significant effect on either cell viability or morphology. The expression of adipogenic markers was evaluated by Western blot. Menadione-induced OS caused a significant decrease in the expression of PPARγ (95% and 99%, for 20 and 50 μM menadione, respectively), FAS (70% and 88%, for 20 and 50 μM menadione, respectively), C/EBPα (75% and 93%, for 20 and 50 μM menadione, respectively), and FABP4 (30% for 50 μM menadione). No changes were detected in intracellular triglyceride levels after the incubation in the presence of menadione. However, when the exposure to menadione-dependent OS was extended to 24 h, the intracellular triglyceride content was augmented by 53% and 68% upon the exposure to 20 and 50 μM menadione, respectively. At the same time, ACC (the ratelimiting enzyme in fatty acid synthesis) was activated (32% and 38% decreased phosphorylation, for 20 and 50 μM menadione, respectively). On the other hand, menadione-triggered OS also activated lipolysis (40% for 50 μM menadione). Together, our results show that OS acutely modulates both the expression and activity of different lipo/adipogenic proteins, activating fatty acids’ metabolic turnover, with enhanced lipolysis, which is overcome by fatty acid synthesis, resulting in an increased triglyceride content. Our next goal is the unraveling of the cellular signaling responsible for these metabolic changes observed. Fil: Funk, Melania Iara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina Fil: Conde, Melisa Ailén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina Fil: Alza, Natalia Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina Fil: Uranga, Romina Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina LVI Reunión Anual Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; XV Reunión Anual de Sociedad Argentina de Microbiología General Virtual Argentina Sociedad Argentina de Investigación Bioquímica y Biología Molecular Sociedad Argentina de Microbiología General |
| description |
Obesity is closely related to metabolic disturbances, with the latter majorly caused by adipose tissue dysfunction. Oxidative stress (OS), a major characteristic of dysfunctional adipose tissue, is considered a primary contributing factor to the etiopathogenesis of obesity and associated comorbidities. However, the biochemical mechanisms by which OS alters adipocyte biology still require to be fully uncovered. We have previously demonstrated that menadione, a synthetic vitamer of vitamin K known to generate intracellular oxygen species, impairs adipogenesis by inhibiting the PI3K/Akt pathway. Our goal in this work was to study the effect of menadione-induced OS on mature adipocytes. For this purpose, differentiated 3T3-L1 adipocytes were exposed to menadione (20 and 50 µM) for 5 h, and different biochemical parameters were assessed. The exposure to menadione resulted in increased cell oxidants (65% and 122% of control, for 20 and 50 µM, respectively). However, none of the concentrations of menadione tested had any significant effect on either cell viability or morphology. The expression of adipogenic markers was evaluated by Western blot. Menadione-induced OS caused a significant decrease in the expression of PPARγ (95% and 99%, for 20 and 50 μM menadione, respectively), FAS (70% and 88%, for 20 and 50 μM menadione, respectively), C/EBPα (75% and 93%, for 20 and 50 μM menadione, respectively), and FABP4 (30% for 50 μM menadione). No changes were detected in intracellular triglyceride levels after the incubation in the presence of menadione. However, when the exposure to menadione-dependent OS was extended to 24 h, the intracellular triglyceride content was augmented by 53% and 68% upon the exposure to 20 and 50 μM menadione, respectively. At the same time, ACC (the ratelimiting enzyme in fatty acid synthesis) was activated (32% and 38% decreased phosphorylation, for 20 and 50 μM menadione, respectively). On the other hand, menadione-triggered OS also activated lipolysis (40% for 50 μM menadione). Together, our results show that OS acutely modulates both the expression and activity of different lipo/adipogenic proteins, activating fatty acids’ metabolic turnover, with enhanced lipolysis, which is overcome by fatty acid synthesis, resulting in an increased triglyceride content. Our next goal is the unraveling of the cellular signaling responsible for these metabolic changes observed. |
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2020 |
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2020 |
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Menadione-induced oxidative stress alters lipid metabolism of the mature adipocyte; LVI Reunión Anual Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; XV Reunión Anual de Sociedad Argentina de Microbiología General; Virtual; Argentina; 2020; 44-44 0327-9545 1667-5746 CONICET Digital CONICET |
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