Rate of Atherosclerosis Progression in ApoE−/− Mice Long After Discontinuation of Cola Beverage Drinking

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.

Non-caloric artificial sweeteners and the microbiome: findings and challenges

“…27 In addition to weight gain, both saccharin and aspartame have been associated with impaired glucose homeostasis in mice, 24,28,29 and aspartame was also shown to induce hyperinsulinemia, 25 impaired insulin tolerance 24,28 and worsened atherosclerosis in genetically-susceptible (ApoE ¡/¡ ) mice. 30,31 In contrast, Flatt and colleagues described anti-hyperglycemic and antihyperinsulinemic effects for saccharin in genetically obese (ob/ob) mice, coupled with attenuation of weight gain. 32 In fact, beneficial effects of NAS were at times described to co-occur with detrimental ones in some studies.…”

Exercise Ameliorates Endocrine Pancreas Damage Induced by Chronic Cola Drinking in Rats

“…Nearly for ten years, we have been studying the variety of physiological and morphological alterations found after chronic ingestion of cola beverages in both genetically modified mice and normal rats. We found that chronic cola drinking accelerated aortic atherosclerosis and enlarged atherosclerotic lesions in atherosclerotic mice [ 20 , 21 ]. In healthy rats, chronic cola drinking induced biochemical and echocardiographic changes, namely, dyslipidemia, hyperglycemia, cardiac remodelling with left ventricle hypertrophy and increased cardiac output [ 22 , 23 ].…”

Functional and Morphological Changes in Endocrine Pancreas following Cola Drink Consumption in Rats

“…We have reported the pathophysiological alterations observed in normal rats [ 1 , 2 ] and in atherosclerosis prone mice [ 3 , 4 ] following cola beverages’ long-term drinking. Both sugar-sweetened and artificially sweetened cola beverages caused alterations.…”

“…Notwithstanding that only sugar-sweetened cola consumption resulted in typical metabolic syndrome alterations (obesity, hypertension, hyperglycemia and dyslipidemia) [ 5 ], artificially sweetened cola drinking resulted in alterations as well. Moreover in atherosclerotic prone mice, light cola accelerated the progression of aortic wall injury to a greater extent compared to regular cola [ 4 ]. Along with the changes observed in rats, a pro-oxidative metabolism was suggested based on the decrease in plasma levels of coenzyme Q 10 (CoQ 10 ) and the increase in the ratio of pro-oxidative to antioxidants compounds [ 2 ].…”