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

FARIÑA J; GAGLIARDINO JJ ET AL

CLINICAL SCIENCE (LONDON, ENGLAND : 1979)

PORTLAND PRESS LTD

Lugar: Londres; Año: 2013 vol. 125 p. 87 - 97

0143-5221

We tested the effect of OS (oxidative stress) inhibition in rats fed with 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/-2 mRNAs, ROS (reactive oxygen species) production, NADPH oxidase activity, 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 (homeostasis model of assessment of insulin resistance) values were significantly higher than those of CD. The AAT from FRD rats had larger adipocytes, higher saturated FAs content, higher NADPH oxidase activity, greater ROS production, a distorted FAs 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 a main role in the FRD-induced metabolic syndrome phenotype.