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Background  Atherosclerosis is a major health burden. Metabolic disorders had been associated with large consumption of soft drinks. The rising incidence of atherosclerosis and metabolic alterations warrants the study of long-term soft drink consumption’ effects on metabolism and atherosclerosis in genetic deficiency of apolipoprotein E which typically develops spontaneous atherosclerosis and metabolic alterations.    Methods  ApoE -/-  mice were randomized in 3 groups accordingly 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: W 8 , C 8 , L 8 ). The remaining mice (all groups) drank water for 8 weeks and were euthanized (Washout: W 16 , C 16 , L 16 ). Body weight and food and drink consumption were periodically measured. Blood was collected (biochemistry). At autopsy, transverse aortic sinus sections were serially cut and stained (histomorphometry); livers and kidneys were processed (microscopy). MANOVA (identification of variance factors) was followed by ANOVA and LSD tests (within-factor differences between levels). Conventionally a p< 0.05 was considered significant.    Results  Treatment increased drinking volumes (vs W 8 : 4 fold C 8 , p<0.0001; +47% L 8 , p<0.02). Only C reduced eating amounts (–54%, p<0.05 vs W 8 ). I). Compared with W 8 : C 8  developed hyperglycemia (+43%, p<0.03) and increased non-HDL cholesterol (+54%, p<0.05); L 8  showed decreased glycemia (–15%, p<0.05 vs W 8 ) and increased creatinine (2.5 fold, p<0.04), urea (+74, p<0.03) and aspartate-aminotransferase (2.8 fold, p<0.05). Hypercreatininemia was observed in L 16  (2.7 fold vs W 16 , p<0.05). Hypertriglyceridemia (+91%, p<0.008) and hyperuremia (+68%, p<0.03) developed over time of study (age). II). Treatment caused plaque area increase (vs W 8 : 28% C 8 , p<0.02 and 50% L 8 , p<0.01; vs W 16 : 43% C 16 , p<0.05 and 68% L 16 , p<0.02) and stenosis (vs W 8 : 38% C 8 , p<0.04 and 57% L 8 , p<0.01; vs W 16 : 71% C 16 , p<0.01 and 46% L 16 , p<0.04). Age also caused plaque area increase (56%, p<0.04). Treatment- and age-effects on plaque enlargement were additive.    Conclusion  Cola beverages caused atherosclerotic lesions’ enlargement with metabolic (C) or non metabolic disturbances (L). ApoE -/-  mice were particularly sensitive to L treatment. These findings may likely relate to caramel colorant and non-nutritive sweeteners in cola drinks and have potential implications in particularly sensitive individuals.

Metabolic disturbances and worsening of atherosclerotic lesions in ApoE-/- mice after cola beverages drinking