LONG-TERM SOFT DRINK CONSUMPTION CAUSES ENLARGEMENT OF ATHEROSCLEROTIC LESIONS IN APOE-/- MICE

M OTERO LOSADA; MC LAUGHLIN SANTIAGO; G RODRIGUEZ GRANILLO; A MÜLLER; G OTTAVIANO; M MORIONDO; J CUTRIN; J MILEI

Congreso; 23 European Meeting on Hypertension &Cardiovascular Protection; 2013

LONG-TERM SOFT DRINK CONSUMPTION CAUSES ENLARGEMENT OF ATHEROSCLEROTIC LESIONS IN APOE-/- MICE M. Otero-Losada 1,S. McLoughlin 1,G. Rodríguez-Granillo 1,A. Muller 1,G. Ottaviano 1,M. Moriondo 1,J. Cutrin 1,2,J. Milei 1. 1 Instituto de Investigaciones Cardiológicas (ININCA), UBA-CONICET, Buenos Aires, ARGENTINA, 2 Department of Molecular Biotechnology and Health Sciences, University of Torino, Turin, ITALY The effects of long-term soft drink consumption on general metabolism and atherosclerosis were evaluated in genetic apolipoprotein-E deficiency. Previously we reported metabolic and cardiovascular alterations associated with cola drinking in an eugenic animal model. Methods: ApoE-/- mice were randomized in 3 groups according with free access to: water (W), regular cola (C) or light cola (L). After 8 weeks, 50% of the animals in each group were euthanized (Treatment: W8, C8, L8). The remaining mice (all groups) drank water for another 8 weeks (i.e.: 16 weeks from beginning of the study) and were then euthanized (Washout: W16, C16, L16). Body weight (weekly) and food and drink consumption (twice a week) were measured. Blood was collected for biochemical assays. At autopsy, transverse aortic sinus sections were serially cut and stained for histomorphometry and livers and kidneys were processed for microscopic assessment. Results: Soft drinks treatment increased drinking volumes (C8: 4 fold, p<0.0001; L8: +47%, p<0.02 vs. W8). I). Compared with W8: C8 developed hyperglycemia (+43%, p<0.03) and increased LDL (+54%, p<0.05); L8 had lower glycemia (-15%, p<0.05 vs W8) and increased creatinine (2.5 fold, p<0.04), urea (+74, p<0.03) and aspartate aminotransferase (AST) (2.8 fold, p<0.05). These changes reversed except for persistent hypercreatininemia in L16 (2.7 fold vs W16, p<0.05). Hypertriglyceridemia (+91%, p<0.008) and hyperuremia (+68%, p<0.03) developed over time (age). II). Treatment caused increase in plaque area (vs W8: 28%, p<0.02 in C8 and 50%, p<0.01 in L8; vs W16: 43%, p<0.05 in C16 and 68%, p<0.02 in L16) and stenosis (vs W8: 38%, p<0.04 in C8 and 57%, p<0.01 in L8; vs W16: 71%, p<0.01 in C16 and 46%, p<0.04 in L16). Age was associated with plaque area increase (56%, p<0.04). Conclusion: Cola beverages caused enlargement of atherosclerotic lesions associated with metabolic (C) and non metabolic disturbances (L). ApoE-/- mice were particularly sensitive to L treatment. Caramel colorant and non-nutritive sweeteners in cola beverages might be involved in L effects. Citations: M. Otero-Losada 1,S. McLoughlin 1,G. Rodríguez-Granillo 1,A. Muller 1,G. Ottaviano 1,M. Moriondo 1,J. Cutrin 1,2,J. Milei 1, LONG-TERM SOFT DRINK CONSUMPTION CAUSES ENLARGEMENT OF ATHEROSCLEROTIC LESIONS IN APOE-/- MICE, Journal of Hypertension Volume 31, e-Supplement A, June 2013 ESH 2013 Abstract Book, e552Session: POSTER SESSION P45: ATHEROSCLEROSIS AND INFLAMMATIONDate: Monday, June 17, 2013