title: Antioxidant treatment prevents the development of fructose-induced abdominal adipose tissue dysfunction.
abstract: 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.
authors: CENEXA (UNLP-CONICET LA PLATA, PAHO/WHO Collaborating Centre for Diabetes), National University of La Plata School of Medicine, Argentina.
authors: Juan Pablo
authors: JP
authors: Fariña
authors: María Elisa
authors: ME
authors: García
authors: Ana
authors: A
authors: Alzamendi
authors: Andrés
authors: A
authors: Giovambattista
authors: Carlos Alberto
authors: CA
authors: Marra
authors: Eduardo
authors: E
authors: Spinedi
authors: Juan José
authors: JJ
authors: Gagliardino
mesh_terms: D050153:Abdominal Fat / Q000378:metabolism*; D000098:Acetophenones / Q000494:pharmacology; D017667:Adipocytes / Q000473:pathology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D015415:Biomarkers / Q000097:blood; D001835:Body Weight; D004435:Eating; D005227:Fatty Acids / Q000378:metabolism*; D005632:Fructose / Q000009:adverse effects*; D006706:Homeostasis; D020738:Leptin / Q000097:blood*; D008297:Male; D008659:Metabolic Diseases / Q000139:chemically induced* / Q000473:pathology; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013549:Sweetening Agents / Q000009:adverse effects*
chemical_list: D000098:Acetophenones; D000975:Antioxidants; D015415:Biomarkers; D005227:Fatty Acids; D020738:Leptin; D013549:Sweetening Agents; D005632:Fructose; C056165:acetovanillone; D019255:NADPH Oxidases