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

Juan Pablo Fariña, María Elisa García, Ana Alzamendi, Andrés Giovambattista, Carlos Alberto Marra, Eduardo Spinedi, Juan José Gagliardino

CENEXA (UNLP-CONICET LA PLATA, PAHO/WHO Collaborating Centre for Diabetes), National University of La Plata School of Medicine, Argentina.

Clinical science (London, England : 1979) 2013 Jul 1

filter terms:

In the present study, we tested the effect of OS (oxidative stress) inhibition in rats fed on an 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, LEP (leptin) and IRS (insulin receptor substrate)-1/IRS-2 mRNAs, ROS (reactive oxygen species) production, NADPH oxidase activity and LEP release by isolated AAT adipocytes. FRD-fed rats had larger AAT mass without changes in body weight, and higher plasma levels of TAG (triacylglycerol), FAs, TBARS (thiobarbituric acid-reactive substance) and LEP. Although no significant changes in glucose and insulin plasma levels were observed in these animals, their HOMA-IR (homoeostasis model assessment of insulin resistance) values were significantly higher than those of CD. The AAT from FRD-fed rats had larger adipocytes, higher saturated FA content, higher NADPH oxidase activity, greater ROS production, a distorted FA content/release pattern, lower insulin sensitivity together with higher and lower mRNA content of LEP and IRS-1-/2 respectively, and released a larger amount 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 APO treatment prevented both changes in NADPH oxidase activity and the development of all the FRD-induced AAT dysfunctions in normal rats strongly suggests that OS plays an important role in the FRD-induced MS (metabolic syndrome) phenotype.

Citation

Juan Pablo Fariña, María Elisa García, Ana Alzamendi, Andrés Giovambattista, Carlos Alberto Marra, Eduardo Spinedi, Juan José Gagliardino. Antioxidant treatment prevents the development of fructose-induced abdominal adipose tissue dysfunction. Clinical science (London, England : 1979). 2013 Jul 1;125(2):87-97