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

• Published in: PPAR Research 2012-01, Vol.2012 (2012), p.140-148
• Main Authors: García, María E., Alzamendi, Ana, Spinedi, Eduardo, Gagliardino, Juan J., Rebolledo, Oscar R., Giovambattista, Andrés
• Format: Article
• Language: English
• Subjects: Adipose tissues; Body fat; Diet; Fructose; Health aspects; Insulin; Leptin; Metabolites; Physiological aspects; Plasma; Rodents
• ISSN: 1687-4757; 1687-4765
• DOI: 10.1155/2012/259093

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.