Effect of red wine on adipocytokine expression and vascular alterations in fructose-fed rats.
BACKGROUND
Imbalance in adipocytokines secretion is related to the development of metabolic syndrome (MS). In addition, moderate consumption of red wine (RW) decreases the risk of cardiovascular disease. The aim of this study was to evaluate the effects of moderate consumption of RW or ethanol (E) on adiponectin and resistin expression, and vascular alterations in fructose-fed rats (FFRs) as an experimental model of MS.


METHODS
Thirty-day-old male Wistar rats were assigned to control (C), F (10% fructose in drinking water), F+E (4.5 ml/kg), and F+RW (35 ml/kg of Malbec RW containing 4.5 ml/kg E). E and RW were administered during the last 4 weeks of a 10-week period.


RESULTS
RW administration to F rats was able to significantly decrease insulin resistance, mesenteric adipose tissue weight, and systolic blood pressure (SBP) compared to F group. F+E only reduced the SBP (P < 0.05 vs. F). F+RW also reduced aortic NAD(P)H-oxidase activity, NAD(P)H subunits Nox4 expression in mesenteric tissue, plasma thiobarbituric acid reactive substances (TBARS), and recovered plasma total antioxidant activity (TAA) compared to F and F+E groups (P < 0.05). Adiponectin expression decreased, whereas resistin, vascular cell adhesion molecules-1 (VCAM-1), and nuclear factor-κB (NF-κB) expression and vascular remodeling in mesenteric arteries were higher in F than in C group (P < 0.05). Only RW was able to partially reverse the aforementioned alterations.


CONCLUSIONS
In this study, Malbec RW, but not alcohol alone, improved the balance of adipocytokines and attenuated the oxidative stress and vascular inflammation in a model of MS, suggesting that nonalcohol components of RW are responsible for the beneficial effects.
Vazquez-Prieto
Marcela A
MA
Department of Pathology, National University of Cuyo, Mendoza, Argentina.
Renna
Nicolás F
NF
Diez
Emiliano R
ER
Cacciamani
Valeria
V
Lembo
Carina
C
Miatello
Roberto M
RM
D050153:Abdominal Fat / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D054392:Adipokines / Q000378:metabolism*; D052242:Adiponectin / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D001794:Blood Pressure; D019422:Dietary Sucrose; D004195:Disease Models, Animal; D000431:Ethanol / Q000008:administration & dosage; D005632:Fructose; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D052243:Resistin / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D014920:Wine
D054392:Adipokines; D052242:Adiponectin; C499920:Adipoq protein, rat; D000975:Antioxidants; D019422:Dietary Sucrose; D016328:NF-kappa B; D052243:Resistin; C499622:Retn protein, rat; D017392:Thiobarbituric Acid Reactive Substances; D019010:Vascular Cell Adhesion Molecule-1; D005632:Fructose; D000431:Ethanol; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases; C498911:Nox4 protein, rat