Instituto de Investigaciones Cardiológicas Prof, Dr, Alberto C, Taquini (ININCA), Facultad de Medicina, Universidad de Buenos Aires (UBA)-Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
Cardiovasc Diabetol. 2013 Apr 1;12:57. doi: 10.1186/1475-2840-12-57.
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.
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 (
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.
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.
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.
动脉粥样硬化是一个主要的健康负担。代谢紊乱与大量饮用软饮料有关。动脉粥样硬化发病率的上升和代谢改变需要研究长期饮用软饮料对载脂蛋白 E 基因缺陷(通常会自发发展为动脉粥样硬化和代谢改变)小鼠代谢和动脉粥样硬化的影响。
将 ApoE-/- 小鼠随机分为 3 组,分别自由饮用:水(W)、普通可乐(C)或低卡可乐(L)。8 周后,每组 50%的动物被安乐死(处理:W8、C8、L8)。其余的老鼠(所有组)继续饮用 8 周的水并被安乐死(Washout:W16、C16、L16)。定期测量体重、食物和饮料的摄入量。采集血液(生化)。解剖时,对主动脉窦进行连续切片和染色(组织形态计量学);处理肝脏和肾脏(显微镜检查)。进行 MANOVA(方差因素的识别),然后进行 ANOVA 和 LSD 检验(各水平之间的差异)。通常,p<0.05 被认为具有统计学意义。
与 W8 相比,处理增加了饮水量(C8:4 倍,p<0.0001;L8:+47%,p<0.02)。只有 C 减少了进食量(-54%,p<0.05 与 W8 相比)。I)与 W8 相比:C8 导致高血糖(+43%,p<0.03)和非高密度脂蛋白胆固醇增加(+54%,p<0.05);L8 显示血糖降低(-15%,p<0.05 与 W8 相比)和肌酐增加(2.5 倍,p<0.04)、尿素(+74%,p<0.03)和天门冬氨酸转氨酶(2.8 倍,p<0.05)。L16 时观察到高肌酸血症(2.7 倍,与 W16 相比,p<0.05)。高脂血症(+91%,p<0.008)和高尿酸血症(+68%,p<0.03)随研究时间(年龄)的增加而发展。II)处理导致斑块面积增加(与 W8 相比:C8:28%,p<0.02 和 50%,p<0.01;L8:43%,p<0.05 和 68%,p<0.02;与 W16 相比:C16:38%,p<0.04 和 57%,p<0.01;L16:71%,p<0.01 和 46%,p<0.04)和狭窄(与 W8 相比:C8:38%,p<0.04 和 57%,p<0.01;L8:71%,p<0.01 和 46%,p<0.04;与 W16 相比:C16:71%,p<0.01 和 46%,p<0.04)。年龄也导致斑块面积增加(56%,p<0.04)。处理和年龄对斑块增大的影响是相加的。
可乐饮料导致动脉粥样硬化病变增大,伴有代谢(C)或非代谢紊乱(L)。ApoE-/- 小鼠对 L 治疗特别敏感。这些发现可能与可乐饮料中的焦糖色素和非营养性甜味剂有关,并可能对特别敏感的个体具有潜在影响。