Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction
- Autores
- Alzamendi, Ana; Giovambattista, Andrés; Garcia, María Elisa; Rebolledo, Oscar R.; 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.
- Materia
-
Biología Celular, Microbiología
fructose rich diet
endocrine abdominal tissue dysfunction - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
- OAI Identificador
- oai:digital.cic.gba.gob.ar:11746/7076
Ver los metadatos del registro completo
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spelling |
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue DysfunctionAlzamendi, AnaGiovambattista, AndrésGarcia, María ElisaRebolledo, Oscar R.Gagliardino, Juan JoséSpinedi, EduardoBiología Celular, Microbiologíafructose rich dietendocrine 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.Hindawi Publishing Corporation2012info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://digital.cic.gba.gob.ar/handle/11746/7076enginfo:eu-repo/semantics/altIdentifier/doi/10.1155/2012/259093info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/reponame:CIC Digital (CICBA)instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Airesinstacron:CICBA2025-09-04T09:43:41Zoai:digital.cic.gba.gob.ar:11746/7076Institucionalhttp://digital.cic.gba.gob.arOrganismo científico-tecnológicoNo correspondehttp://digital.cic.gba.gob.ar/oai/snrdmarisa.degiusti@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:94412025-09-04 09:43:41.627CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Airesfalse |
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 Biología Celular, Microbiología 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 Garcia, María Elisa Rebolledo, Oscar R. Gagliardino, Juan José Spinedi, Eduardo |
author |
Alzamendi, Ana |
author_facet |
Alzamendi, Ana Giovambattista, Andrés Garcia, María Elisa Rebolledo, Oscar R. Gagliardino, Juan José Spinedi, Eduardo |
author_role |
author |
author2 |
Giovambattista, Andrés Garcia, María Elisa Rebolledo, Oscar R. Gagliardino, Juan José Spinedi, Eduardo |
author2_role |
author author author author author |
dc.subject.none.fl_str_mv |
Biología Celular, Microbiología fructose rich diet endocrine abdominal tissue dysfunction |
topic |
Biología Celular, Microbiología 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. |
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 http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
https://digital.cic.gba.gob.ar/handle/11746/7076 |
url |
https://digital.cic.gba.gob.ar/handle/11746/7076 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.1155/2012/259093 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Hindawi Publishing Corporation |
publisher.none.fl_str_mv |
Hindawi Publishing Corporation |
dc.source.none.fl_str_mv |
reponame:CIC Digital (CICBA) instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Aires instacron:CICBA |
reponame_str |
CIC Digital (CICBA) |
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CIC Digital (CICBA) |
instname_str |
Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
instacron_str |
CICBA |
institution |
CICBA |
repository.name.fl_str_mv |
CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
repository.mail.fl_str_mv |
marisa.degiusti@sedici.unlp.edu.ar |
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12.623145 |