Lipid profile and plasma antioxidant status in sweet carbonated beverage-induced metabolic syndrome in rat

Otero‐Losada, Matilde; Grana, Daniel; Müller, Angélica; Ottaviano, G; Ambrosio, Giuseppe; Milei, José

doi:10.1016/j.ijcard.2010.09.066

Cited by 24 publications

(32 citation statements)

References 12 publications

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“…W12 vs W6). As observed previously in relation to the antioxidant concentration in plasma, long-term hypercaloric consumption resulted in changes similar to those found as a result of normal aging [6] . Both cola beverages induced an increase in LVDD, EDV and ESV, accompanied by a reduction in relative wall thickness.…”

Section: Discussionsupporting

confidence: 87%

“…No differences in plasma CoQ10 concentration were found across groups after washout (F2,16 = 2.379, NS), though W rats had 46% lower levels compared with those at baseline (F1,34 = 5.197, P < 0.03) [6] . Treatment did not modify plasma levels of α-tocopherol at any time (F1,34 = 2.018, NS) although, similar to that observed for CoQ10, plasma levels of α-tocopherol decreased by 48% (F1,34 = 4.532, P < 0.04) in the W group at the end of the washout period compared with levels found in the same group at baseline [6] . Consumption of cola drinks had no significant effect on uricemia (data not shown).…”

Section: Plasma Biochemistrymentioning

confidence: 82%

“…Plasma concentrations of coenzyme Q10 and α-tocopherol were determined by HPLC-RP with UV detection using Waters 1500 Series, HPLC binary pump, Waters 717 plus Autosampler, Symmetry C18 4.6 mm × 150 mm and 5 μm particle size column, guard column 4 mm × 4 mm (5 μm), Waters 2487 Dual λ Absorbance Detector, and Waters 2465 Electrochemical Detector. Waters Breeze™ Chromatography Data System software version for Windows NT was used for data acquisition and storage [6] . Blood pressure determination SBP was measured by tail cuff plethysmography in unanesthetized rats restrained in a plastic chamber.…”

Section: Biochemical Determinationsmentioning

confidence: 99%

“…Recently, we have demonstrated that most features of metabolic syndrome can be replicated in an experimental model of soft drink consumption. Body weight gain, hypertension, decreased food intake, hyperglycemia, hypertriglyceridemia, and a tendency to hypercholesterolemia were found after chronic consumption of regular (sucrose-sweetened) cola beverage in rats [6] . As a logical extension to that earlier report, the present paper aimed to investigate possible biochemical, echocardiographic and pathological alterations associated with chronic consumption of cola beverage in rats.…”

Section: Introductionmentioning

confidence: 95%

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Chronic cola drinking induces metabolic and cardiac alterations in rats

Milei

Losada²,

Llambí³

et al. 2011

WJC

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AIM:To investigate the effects of chronic drinking of cola beverages on metabolic and echocardiographic parameters in rats. METHODS:Forty-eight male Wistar rats were divided in 3 groups and allowed to drink regular cola (C), diet cola (L), or tap water (W) ad libitum during 6 mo. After this period, 50% of the animals in each group were euthanized. The remaining rats drank tap water ad libitum for an additional 6 mo and were then sacrificed. Rat weight, food, and beverage consumption were measured regularly. Biochemical, echocardiographic and systolic blood pressure data were obtained at baseline, and at 6 mo (treatment) and 12 mo (washout). A complete histopathology study was performed after sacrifice. RESULTS:After 6 mo, C rats had increased body weight (+7%, P < 0.01), increased liquid consumption (+69%, P < 0.001), and decreased food intake (-31%, P < 0.001). C rats showed mild hyperglycemia and hypertriglyceridemia. Normoglycemia (+69%, P < 0.01) and sustained hypertriglyceridemia (+69%, P < 0.01) were observed in C after washout. Both cola beverages induced an increase in left ventricular diastolic diameter (C: +9%, L: +7%, P < 0.05 vs W) and volumes (diastolic C: +26%, L: +22%, P < 0.01 vs W; systolic C: +24%, L: +24%, P < 0.05 vs W) and reduction of relative posterior wall thickness (C: -8%, L: -10%, P < 0.05 vs W). Cardiac output tended to increase (C: +25%, P < 0.05 vs W; L: +17%, not significant vs W). Heart rate was not affected. Pathology findings were scarce, related to aging rather than treatment.CONCLUSION: This experimental model may prove useful to investigate the consequences of high consumption of soft drinks.

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Section: Discussionsupporting

confidence: 87%

Section: Plasma Biochemistrymentioning

confidence: 82%

Section: Biochemical Determinationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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Chronic cola drinking induces metabolic and cardiac alterations in rats

Milei

Losada²,

Llambí³

et al. 2011

WJC

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“…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]. We have reported the development of metabolic syndrome after long-term cola beverages consumption in rats [8], [9]. Hypertension, hyperglycemia, increased body weight, dyslipidemia and echocardiographic alterations were observed while pathology findings were scarce, related to aging rather than treatment [8], [9].…”

Section: Introductionmentioning

confidence: 86%

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

et al. 2014

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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.

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