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

J MILEI; M OTERO LOSADA; DR GRANA; A MÜLLER; G OTTAVIANO; G AMBROSIO

Oslo, Norway

Congreso; 20th European Meeting on Hypertension; 2010

European Society of Hypertension

  Oxidative stress is involved in the pathophysiology and cardiovascular complications of metabolic syndrome. Objective: To investigate changes in plasma profile of biomarkers of altered redox mechanisms and lipid metabolism, associated with experimentallyinduced metabolic syndrome.Methods: Forty-eight male Wistar rats were allowed to drink ad libitum: 1) regular cola (sucrose-sweetened carbonated drink); 2) diet cola (non-nutritive sweetener containing, low-calorie carbonated drink); 3) tap water (controls). After 6 months, all groups were switched to an additional 6 months of tap water drinking (wash-out). Plasma concentrations of the endogenous antioxidants a-tocopherol and ubiquinone-10 were measured using RPHPLC with UV detection. Plasma concentrations of glucose, triglycerides,total cholesterol and HDL-cholesterol were measured by standard enzymatic methods. Determinations were performed at 6 months (end of treatment) and 12 months (end of wash-out). Results: In group 1, 6 months of sucrose-sweetened beverage drinking led to significant weight gain (71%, p<0.01), hypertension (7.50.5% increase in systolic blood pressure, p<0.01), hypertriglyceridemia (3-fold, p<0.01), hyperglycemia (151%, p<0.05), and low ubiquinone-10 levels (522% decrease, p<0.05). Light cola-drinking rats showed normoglycemia, but an unexpected tendency to hypertriglyceridemia (2-fold, N.S.) and hypercholesterolemia (29% increase in total cholesterol, N.S.); CoQ10 levels were slightly decreased compared to controls (27%, N.S.), but higher than group 1 (51% increase, N.S). These metabolic alterations reversed after wash-out, except for hypertriglyceridemia and low ubiquinone-10 levels. Interestingly, by this time decreased a-tocopherol concentrations and hypercholesterolemia were observed in all 3 groups (i.e., unrelated to treatment). Conclusions: Experimentally-induced metabolic syndrome induces oxidative stress-related biochemical changes; some of these alterations may be shared by the natural aging process.Objective: To investigate changes in plasma profile of biomarkers of altered redox mechanisms and lipid metabolism, associated with experimentallyinduced metabolic syndrome.Methods: Forty-eight male Wistar rats were allowed to drink ad libitum: 1) regular cola (sucrose-sweetened carbonated drink); 2) diet cola (non-nutritive sweetener containing, low-calorie carbonated drink); 3) tap water (controls). After 6 months, all groups were switched to an additional 6 months of tap water drinking (wash-out). Plasma concentrations of the endogenous antioxidants a-tocopherol and ubiquinone-10 were measured using RPHPLC with UV detection. Plasma concentrations of glucose, triglycerides,total cholesterol and HDL-cholesterol were measured by standard enzymatic methods. Determinations were performed at 6 months (end of treatment) and 12 months (end of wash-out). Results: In group 1, 6 months of sucrose-sweetened beverage drinking led to significant weight gain (71%, p<0.01), hypertension (7.50.5% increase in systolic blood pressure, p<0.01), hypertriglyceridemia (3-fold, p<0.01), hyperglycemia (151%, p<0.05), and low ubiquinone-10 levels (522% decrease, p<0.05). Light cola-drinking rats showed normoglycemia, but an unexpected tendency to hypertriglyceridemia (2-fold, N.S.) and hypercholesterolemia (29% increase in total cholesterol, N.S.); CoQ10 levels were slightly decreased compared to controls (27%, N.S.), but higher than group 1 (51% increase, N.S). These metabolic alterations reversed after wash-out, except for hypertriglyceridemia and low ubiquinone-10 levels. Interestingly, by this time decreased a-tocopherol concentrations and hypercholesterolemia were observed in all 3 groups (i.e., unrelated to treatment). Conclusions: Experimentally-induced metabolic syndrome induces oxidative stress-related biochemical changes; some of these alterations may be shared by the natural aging process.