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

FARIÑA J; GARCIA, ME; ALZAMENDI, A; GIOVAMBATTISTA A; MARRA, C; SPINEDI, E; GAGLIARDINO, JUAN J

CLINICAL SCIENCE (LONDON, ENGLAND : 1979)

PORTLAND PRESS LTD

Lugar: Londres; Año: 2013 p. 87 - 97

0143-5221

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 anFRD 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 andcell size, FA (fatty acid) composition (content and release), OS status, LEP (leptin) and IRS (insulin receptorsubstrate)-1/IRS-2 mRNAs, ROS (reactive oxygen species) production, NADPH oxidase activity and LEP release byisolated AAT adipocytes. FRD-fed rats had larger AAT mass without changes in body weight, and higher plasmalevels of TAG (triacylglycerol), FAs, TBARS (thiobarbituric acid-reactive substance) and LEP. Although no significantchanges in glucose and insulin plasma levels were observed in these animals, their HOMA-IR (homoeostasis modelassessment of insulin resistance) values were significantly higher than those of CD. The AAT from FRD-fed rats hadlarger adipocytes, higher saturated FA content, higher NADPH oxidase activity, greater ROS production, a distortedFA content/release pattern, lower insulin sensitivity together with higher and lower mRNA content of LEP andIRS-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. Thefact that APO treatment prevented both changes in NADPH oxidase activity and the development of all theFRD-induced AAT dysfunctions in normal rats strongly suggests that OS plays an important role in the FRD-inducedMS (metabolic syndrome) phenotype.