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.
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July 2013
Research Article|
March 26 2013
Antioxidant treatment prevents the development of fructose-induced abdominal adipose tissue dysfunction
Juan Pablo Fariña;
Juan Pablo Fariña
1
*CENEXA (UNLP-CONICET LA PLATA, PAHO/WHO Collaborating Centre for Diabetes), National University of La Plata School of Medicine, La Plata, Argentina
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María Elisa García;
María Elisa García
1
*CENEXA (UNLP-CONICET LA PLATA, PAHO/WHO Collaborating Centre for Diabetes), National University of La Plata School of Medicine, La Plata, Argentina
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Ana Alzamendi;
Ana Alzamendi
†Neuroendocrine Unit, IMBICE (CICPBA-CONICET LA PLATA) La Plata, Argentina
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Andrés Giovambattista;
Andrés Giovambattista
†Neuroendocrine Unit, IMBICE (CICPBA-CONICET LA PLATA) La Plata, Argentina
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Carlos Alberto Marra;
Carlos Alberto Marra
‡INIBIOLP (UNLP-CONICET LA PLATA), National University of La Plata School of Medicine, La Plata, Argentina
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Eduardo Spinedi;
Eduardo Spinedi
†Neuroendocrine Unit, IMBICE (CICPBA-CONICET LA PLATA) La Plata, Argentina
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Juan José Gagliardino
*CENEXA (UNLP-CONICET LA PLATA, PAHO/WHO Collaborating Centre for Diabetes), National University of La Plata School of Medicine, La Plata, Argentina
Correspondence: Dr Juan J. Gagliardino (email direccion@cenexa.org).
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Clin Sci (Lond) (2013) 125 (2): 87–97.
Article history
Received:
August 30 2012
Revision Received:
November 29 2012
Accepted:
February 06 2013
Accepted Manuscript online:
February 06 2013
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. Clin Sci (Lond) 1 July 2013; 125 (2): 87–97. doi: https://doi.org/10.1042/CS20120470
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