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Artículo

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

Fariña, Juan Pablo; Garcia, Maria Elisa; Alzamendi, AnaIcon ; Giovambattista, AndresIcon ; Marra, Carlos AlbertoIcon ; Spinedi, Eduardo JulioIcon ; Gagliardino, Juan JoseIcon
Fecha de publicación: 02/2013
Editorial: Portland Press
Revista: Clinical Science
ISSN: 0143-5221
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Medicina General e Interna

Resumen

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.
Palabras clave: Adipokines , Abdominal Adipocytes , Lipid Metabolism , Insulin Signaling
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/5292
URL: http://www.clinsci.org/content/125/2/87
DOI: http://dx.doi.org/ 10.1042/CS20120470
DOI: http://dx.doi.org/10.1042/CS20120470
Colecciones
Articulos(CENEXA)
Articulos de CENTRO DE ENDOCRINOLOGIA EXP.Y APLICADA (I)
Articulos(IMBICE)
Articulos de INST.MULTIDISCIPL.DE BIOLOGIA CELULAR (I)
Articulos(INIBIOLP)
Articulos de INST.DE INVEST.BIOQUIMICAS DE LA PLATA
Citación
Fariña, Juan Pablo; Garcia, Maria Elisa; Alzamendi, Ana; Giovambattista, Andres; Marra, Carlos Alberto; et al.; Antioxidant treatment prevents the development of fructose-induced abdominal adipose tissue dysfunction; Portland Press; Clinical Science; 125; 2; 2-2013; 87-97
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