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

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

CARDIOVASCULAR DIABETOLOGY

BIOMED CENTRAL LTD

Lugar: Londres; Año: 2013 vol. 12 p. 1 - 7

1475-2840

Metabolic disturbances and worsening of atherosclerotic lesions in ApoE-/- mice after cola beverages drinking Matilde E Otero-Losada1*, Santiago Mc Loughlin1, Gastón Rodríguez-Granillo1, Angélica Müller1, Graciela Ottaviano1, Marisa Moriondo1, Juan C Cutrin1,2 and José Milei1* * Corresponding authors: Matilde E Otero-Losada mol@fmed.uba.ar - José Milei ininca@fmed.uba.ar Author Affiliations For all author emails, please log on. Cardiovascular Diabetology 2013, 12:57 doi:10.1186/1475-2840-12-57 Published: 1 April 2013 Abstract 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: W8, C8, L8). The remaining mice (all groups) drank water for 8 weeks and were euthanized (Washout: W16, C16, L16). 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 W8: 4 fold C8, p<0.0001; +47% L8, p<0.02). Only C reduced eating amounts (?54%, p<0.05 vs W8). I). Compared with W8: C8 developed hyperglycemia (+43%, p<0.03) and increased non-HDL cholesterol (+54%, p<0.05); L8 showed decreased glycemia (?15%, p<0.05 vs W8) 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 L16 (2.7 fold vs W16, 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 W8: 28% C8, p<0.02 and 50% L8, p<0.01; vs W16: 43% C16, p<0.05 and 68% L16, p<0.02) and stenosis (vs W8: 38% C8, p<0.04 and 57% L8, p<0.01; vs W16: 71% C16, p<0.01 and 46% L16, 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. Keywords: Atherosclerosis; Soft drinks; Glycemia; Urea; Creatinine; Plaque area; Apo-E deficiency