Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction
- Autores
- Alzamendi, Ana; Giovambattista, Andrés; García, María Elisa; Rebolledo, Oscar Remigio; Gagliardino, Juan José; Spinedi, Eduardo
- Año de publicación
- 2012
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Aim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology. Adult normal male rats received a standard commercial diet (CD) or FRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25mg/Kg BW/day; CD-PIO and FRD-PIO). Thereafter, we measured circulating metabolic, endocrine, and oxidative stress (OS) markers, abdominal adipose tissue (AAT) mass, leptin (LEP) and plasminogen activator inhibitor-1 (PAI-1) tissue content/expression, and leptin release by isolated adipocytes incubated with different concentrations of insulin. Results. Plasma glucose, insulin, triglyceride, TBARS, LEP, and PAI-1 levels were higher in FRD rats; PIO coadministration fully prevented all these increments. AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP, and displayed decreased sensitivity to insulin stimulation; these effects were significantly ameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increased significantly in FRD rats, those of insulin-receptor-substrate- (IRS-) 1 and IRS-2 were reduced. PIO coadministration prevented FRD effects on LEP, PAI-1, and IRS-2 (fully) and IRS-1 (partially) mRNAs in AAT. Conclusion. PPARγ would play a relevant role in the development of the FRD-induced metabolicendocrine dysfunction.
Facultad de Ciencias Médicas - Materia
-
Medicina
Microbiología
Adiposidad
Fructosa
fructose rich diet, endocrine abdominal tissue dysfunction - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/68072
Ver los metadatos del registro completo
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Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue DysfunctionAlzamendi, AnaGiovambattista, AndrésGarcía, María ElisaRebolledo, Oscar RemigioGagliardino, Juan JoséSpinedi, EduardoMedicinaMicrobiologíaAdiposidadFructosafructose rich diet, endocrine abdominal tissue dysfunctionAim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology. Adult normal male rats received a standard commercial diet (CD) or FRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25mg/Kg BW/day; CD-PIO and FRD-PIO). Thereafter, we measured circulating metabolic, endocrine, and oxidative stress (OS) markers, abdominal adipose tissue (AAT) mass, leptin (LEP) and plasminogen activator inhibitor-1 (PAI-1) tissue content/expression, and leptin release by isolated adipocytes incubated with different concentrations of insulin. Results. Plasma glucose, insulin, triglyceride, TBARS, LEP, and PAI-1 levels were higher in FRD rats; PIO coadministration fully prevented all these increments. AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP, and displayed decreased sensitivity to insulin stimulation; these effects were significantly ameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increased significantly in FRD rats, those of insulin-receptor-substrate- (IRS-) 1 and IRS-2 were reduced. PIO coadministration prevented FRD effects on LEP, PAI-1, and IRS-2 (fully) and IRS-1 (partially) mRNAs in AAT. Conclusion. PPARγ would play a relevant role in the development of the FRD-induced metabolicendocrine dysfunction.Facultad de Ciencias Médicas2012info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/68072enginfo:eu-repo/semantics/altIdentifier/url/https://www.hindawi.com/journals/ppar/2012/259093/info:eu-repo/semantics/altIdentifier/issn/1687-4765info:eu-repo/semantics/altIdentifier/doi/10.1155/2012/259093info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-03T10:42:30Zoai:sedici.unlp.edu.ar:10915/68072Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 10:42:31.037SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
title |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
spellingShingle |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction Alzamendi, Ana Medicina Microbiología Adiposidad Fructosa fructose rich diet, endocrine abdominal tissue dysfunction |
title_short |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
title_full |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
title_fullStr |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
title_full_unstemmed |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
title_sort |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction |
dc.creator.none.fl_str_mv |
Alzamendi, Ana Giovambattista, Andrés García, María Elisa Rebolledo, Oscar Remigio Gagliardino, Juan José Spinedi, Eduardo |
author |
Alzamendi, Ana |
author_facet |
Alzamendi, Ana Giovambattista, Andrés García, María Elisa Rebolledo, Oscar Remigio Gagliardino, Juan José Spinedi, Eduardo |
author_role |
author |
author2 |
Giovambattista, Andrés García, María Elisa Rebolledo, Oscar Remigio Gagliardino, Juan José Spinedi, Eduardo |
author2_role |
author author author author author |
dc.subject.none.fl_str_mv |
Medicina Microbiología Adiposidad Fructosa fructose rich diet, endocrine abdominal tissue dysfunction |
topic |
Medicina Microbiología Adiposidad Fructosa fructose rich diet, endocrine abdominal tissue dysfunction |
dc.description.none.fl_txt_mv |
Aim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology. Adult normal male rats received a standard commercial diet (CD) or FRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25mg/Kg BW/day; CD-PIO and FRD-PIO). Thereafter, we measured circulating metabolic, endocrine, and oxidative stress (OS) markers, abdominal adipose tissue (AAT) mass, leptin (LEP) and plasminogen activator inhibitor-1 (PAI-1) tissue content/expression, and leptin release by isolated adipocytes incubated with different concentrations of insulin. Results. Plasma glucose, insulin, triglyceride, TBARS, LEP, and PAI-1 levels were higher in FRD rats; PIO coadministration fully prevented all these increments. AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP, and displayed decreased sensitivity to insulin stimulation; these effects were significantly ameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increased significantly in FRD rats, those of insulin-receptor-substrate- (IRS-) 1 and IRS-2 were reduced. PIO coadministration prevented FRD effects on LEP, PAI-1, and IRS-2 (fully) and IRS-1 (partially) mRNAs in AAT. Conclusion. PPARγ would play a relevant role in the development of the FRD-induced metabolicendocrine dysfunction. Facultad de Ciencias Médicas |
description |
Aim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology. Adult normal male rats received a standard commercial diet (CD) or FRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25mg/Kg BW/day; CD-PIO and FRD-PIO). Thereafter, we measured circulating metabolic, endocrine, and oxidative stress (OS) markers, abdominal adipose tissue (AAT) mass, leptin (LEP) and plasminogen activator inhibitor-1 (PAI-1) tissue content/expression, and leptin release by isolated adipocytes incubated with different concentrations of insulin. Results. Plasma glucose, insulin, triglyceride, TBARS, LEP, and PAI-1 levels were higher in FRD rats; PIO coadministration fully prevented all these increments. AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP, and displayed decreased sensitivity to insulin stimulation; these effects were significantly ameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increased significantly in FRD rats, those of insulin-receptor-substrate- (IRS-) 1 and IRS-2 were reduced. PIO coadministration prevented FRD effects on LEP, PAI-1, and IRS-2 (fully) and IRS-1 (partially) mRNAs in AAT. Conclusion. PPARγ would play a relevant role in the development of the FRD-induced metabolicendocrine dysfunction. |
publishDate |
2012 |
dc.date.none.fl_str_mv |
2012 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion Articulo http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://sedici.unlp.edu.ar/handle/10915/68072 |
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http://sedici.unlp.edu.ar/handle/10915/68072 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
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info:eu-repo/semantics/altIdentifier/url/https://www.hindawi.com/journals/ppar/2012/259093/ info:eu-repo/semantics/altIdentifier/issn/1687-4765 info:eu-repo/semantics/altIdentifier/doi/10.1155/2012/259093 |
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info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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openAccess |
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http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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