Cardiorenal involvement in metabolic Syndrome Induced by Cola Drinking in Rats: Proinflammatory Cytokines and Impaired Antioxidative Protection

OTERO-LOSADA, MATILDE; GOMEZ LLAMBI H; OTTAVIANO G; CAO G; MULLER A; F. AZZATO; AMBROSIO G; J MILEI

MEDIATORS OF INFLAMMATION

HINDAWI PUBLISHING CORPORATION

Lugar: New York; Año: 2016 p. 1 - 11

0962-9351

We report experimental evidence confirming renal histopathology, proinflammatory mediators, and oxidative metabolism inducedby cola drinking. Male Wistar rats drank ad libitum regular cola (C, 𝑛 = 12) or tap water (W, 𝑛 = 12). Measures. Bodyweight, nutritional data, plasma glucose, cholesterol fractions, TG, urea, creatinine, coenzyme Q10, SBP, and echocardiograms(0 mo and 6 mo). At 6 months euthanasia was performed. Kidneys were processed for histopathology and immunohistochemistry(semiquantitative). Compared with W, C rats showed (I) overweight (+8%, 𝑝 < 0.05), hyperglycemia (+11%, 𝑝 < 0.05),hypertriglyceridemia (2-fold, 𝑝 < 0.001), higher AIP (2-fold, 𝑝 < 0.01), and lower Q10 level (−55%, 𝑝 < 0.05); (II) increasedLV diastolic diameter (+9%, 𝑝 < 0.05) and volume (systolic +24%, 𝑝 < 0.05), posterior wall thinning (−8%, 𝑝 < 0.05), and largercardiac output (+24%, 𝑝 < 0.05); (III) glomerulosclerosis (+21%, 𝑝 < 0.05), histopathology (+13%, 𝑝 < 0.05), higher tubularexpression of IL-6 (7-fold, 𝑝 < 0.001), and TNF𝛼 (4-fold, 𝑝 < 0.001). (IV) Correlations were found for LV dimensions with IL-6(74%, 𝑝 < 0.001) and TNF𝛼 (52%, 𝑝 < 0.001) and fully abolished after TG and Q10 control. Chronic cola drinking induced cardiacremodeling associated with increase in proinflammatory cytokines and renal damage. Hypertriglyceridemia and oxidative stresswere key factors. Hypertriglyceridemic lipotoxicity in the context of defective antioxidant/anti-inflammatory protection due to lowQ10 level might play a key role in cardiorenal disorder induced by chronic cola drinking in rats.