Abstract
This study was conducted in order to evaluate the effect of cola beverages drinking on atherosclerosisand test the hypothesis whether cola beverages consumption at early life stages might affect the development and progression of atherosclerosis later in life.ApoE−/− C57BL/6J mice (8 week-old) were randomized in 3 groups (n = 20 each) according to free accessto water (W), sucrose sweetened carbonated cola drink(C) or aspartame-acesulfame K sweetened carbonated ‘light’ cola drink (L)for the next 8 weeks. Drinking treatment was ended by switching C and L groups to drinking water. Four mice per group and time were sequentially euthanized: before treatment (8weeks-old), at the end of treatment (16 weeks-old) and after treatment discontinuation (20 weeks-old, 24 weeks-old, 30 week-old mice). Aortic roots and livers were harvested, processed for histology and serial cross-sections were stained. Aortic plaque area was analyzed and plaque/media-ratio was calculated.Early consumption of cola drinks accelerated atherosclerotic plaque progression favoring the interaction between macrophages and myofibroblasts, without the participation of either T lymphocytes or proliferative activity. Plaque/media-ratio varied according to drink treatment (F2,54 = 3.433, p<0.04) and mice age (F4,54 = 5.009, p<0.03) and was higher in C and L groups compared with age-matched W group (p<0.05 at 16 weeks and 20 weeks, p<0.01 at 24 weeks and 30 weeks). Natural evolution of atherosclerosis in ApoE−/− mice (W group) evidenced atherosclerosis acceleration in parallel with a rapid increase in liver inflammation around the 20 weeks of age.Cola drinking within the 8–16 weeks of age accelerated atherosclerosis progression in ApoE−/− mice favoring aortic plaque enlargement (inward remodeling) over media thinning all over the study time. Data suggest that cola drinking at early life stages may predispose to atherosclerosis progression later in life in ApoE−/− mice.
Highlights
Atherosclerosis risk increases with age [1] and unhealthy nutritional habits during childhood and youth have been suggested to favor atherosclerosis complications later in life [2,3]
Longitudinal cohort studies have demonstrated increased cardiovascular risk in adulthood of obese children [4,5] and that exposure to cardiovascular risk factors early in life may contribute to the development of atherosclerosis [6].The increasing consumption of cola beverages has been associated with obesity and a rising incidence of atherosclerosis and cardiovascular disease over the past decades [7]
Mice 20–24 weeks-old of age showed cytoplasmic expression of smooth muscle a-actin and CD68 indicating the coexistence of myofibroblasts and macrophages respectively in the atherosclerotic plaque (Figure 2B, C)
Summary
Atherosclerosis risk increases with age [1] and unhealthy nutritional habits during childhood and youth have been suggested to favor atherosclerosis complications later in life [2,3]. We observed that ApoE2/2C57BL/6J mice exhibited a particular sensitivity to the effects of cola beverage drinking [10]. Arterial pathology was induced bysucrosesweetened cola (C) drinking in association with hyperglycemia [10]. Artificially-sweetened ‘light’ cola(L) drinking induced non-metabolic changes compared with water drinking ApoE2/2 mice [10]. Both C and L drinkingcaused increase in plaque area(28%C, 50% L) and stenosis (38%C, 57% L) at the end of the drinking period [11]. Discontinuation of cola beverages resulted in paradoxical worsening of lesions (increase in plaque area: 43%C, 68% L andstenosis: 71%C, 46% L). Treatment- and age-effects on plaque damage were additive [10]
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