Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction

Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction

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 piog...

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Main Authors: Alzamendi, Ana, Giovambattista, Andrés, García, María E., Rebolledo, Oscar R., Gagliardino, Juan J., Spinedi, Eduardo
Format: Online
Language:English
Published: Hindawi Publishing Corporation 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469242/
id pubmed-3469242
recordtype oai_dc
spelling pubmed-34692422012-10-22 Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction Alzamendi, Ana Giovambattista, Andrés García, María E. Rebolledo, Oscar R. Gagliardino, Juan J. Spinedi, Eduardo Research Article 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. 0.25 mg/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 metabolic-endocrine dysfunction. Hindawi Publishing Corporation 2012 2012-10-02 /pmc/articles/PMC3469242/ /pubmed/23091482 http://dx.doi.org/10.1155/2012/259093 Text en Copyright © 2012 Ana Alzamendi et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Alzamendi, Ana
Giovambattista, Andrés
García, María E.
Rebolledo, Oscar R.
Gagliardino, Juan J.
Spinedi, Eduardo
spellingShingle Alzamendi, Ana
Giovambattista, Andrés
García, María E.
Rebolledo, Oscar R.
Gagliardino, Juan J.
Spinedi, Eduardo
Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose Tissue Dysfunction
author_facet Alzamendi, Ana
Giovambattista, Andrés
García, María E.
Rebolledo, Oscar R.
Gagliardino, Juan J.
Spinedi, Eduardo
author_sort Alzamendi, Ana
title Effect of Pioglitazone on the Fructose-Induced Abdominal Adipose 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
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. 0.25 mg/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 metabolic-endocrine dysfunction.
publisher Hindawi Publishing Corporation
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3469242/
_version_ 1611915412675493888

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