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

ALZAMENDI, A; GIOVAMBATTISTA, A; GARCIA, ME; REBOLLEDO, O; GAGLIARDINO, JUAN J; SPINEDI, E

PPAR research

Hindawi Publishing Corporation

Lugar: New York; Año: 2012 p. 1 - 10

1687-4757

Aim: To test the potential role of PPARγ in the endocrine abdominal tissue dysfunctioninduced by feeding normal rats with a fructose rich diet (FRD) during three weeks.Methodology: Adult normal male rats received a standard commercial diet (CD) orFRD, (10% in drinking water) without or with pioglitazone (PIO) (i.p. 0.25 mg/KgBW/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 ofinsulin. Results: Plasma glucose, insulin, triglyceride, TBARS, LEP and PAI-1 levelswere higher in FRD rats; PIO co-administration fully prevented all these increments.AAT adipocytes from FRD rats were larger, secreted a higher amount of LEP anddisplayed decreased sensitivity to insulin stimulation; these effects were significantlyameliorated by PIO. Whereas AAT LEP and PAI-1 (mRNA) concentrations increasedsignificantly in FRD rats, those of insulin receptor substrate (IRS)-1 and IRS-2 werereduced. PIO co-administration prevented FRD effects on LEP, PAI-1, and IRS-2(fully), and IRS-1 (partially) mRNAs in AAT. Conclusion: PPARγ would play arelevant role in the development of the FRD-induced metabolic-endocrine dysfunction.