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
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/68072
Acceder
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network_name_str SEDICI (UNLP)
spelling 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:UNLP2025-09-29T11:10:30Zoai: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:13292025-09-29 11:10:30.789SEDICI (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
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/68072
url http://sedici.unlp.edu.ar/handle/10915/68072
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 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
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
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reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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