Antioxidant treatment prevents the development of fructose-induced abdominal adipose tissue dysfunction

FARIÑA JP; GARCÍA M.E.; ALZAMENDI, A.; GIOBAMBATTISTA, A.; MARRA CARLOS ALBERTO; SPINEDI, E.; GAGLIARDINO, JUAN JOSÉ

CLINICAL SCIENCE (LONDON, ENGLAND : 1979)

PORTLAND PRESS LTD

Lugar: Londres; Año: 2012

0143-5221

We tested the effect of OS (oxidative stress) inhibition in rats fed with a FRD (fructose-rich diet; 10% w/v in drinking water) for 3 weeks. Normal adult male rats received a standard CD (commercial diet) or an FRD without or with an inhibitor of NADPH-oxidase, APO (apocynin; 5 mM in drinking water; CD-APO and FRD-APO). We thereafter measured plasma OS and metabolic-endocrine markers, AAT (abdominal adipose tissue) mass and cell size, FA (fatty acid) composition (content and release), OS status, mRNAs of LEP (leptin) and IRS (insulin receptor substrate)-1/-2, ROS (reactive oxygen species) production, and LEP release by isolated AAT adipocytes. FRD rats had larger AAT mass without changes in body weight, and higher plasma levels of triglycerides, FAs, TBARS and LEP. While no significant changes in glucose and insulin plasma levels were observed in these animals, their HOMA-IR values were significantly higher than those of CD. The AAT from FRD rats had larger adipocytes, higher content of saturated FAs, greater ROS production, a distorted content/release pattern of FAs, lower insulin sensitivity together with higher and lower mRNA content of LEP and IRS-1-/2, respectively, and it secreted large amounts of LEP. The development of all the clinical, OS, metabolic, endocrine and molecular changes induced by the FRD were significantly prevented by APO co-administration. The fact that co-administration of APO prevents the development of all the FRD-induced abnormal changes in normal rats suggests that OS is the first and main cause of the fructose-induced metabolic syndrome phenotype.