effect of atorvastatin therapy in the adiponectin levels in an animal model of diabetes and...
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eccentric cardiac remodelling, but had no direct effect onglycaemic control. However the increased adiponectin levelspotentially indicate improved insulin signalling.
Keywords: Type II diabetes and obesity; Oxidative stress;Resistance training
doi:10.1016/j.yjmcc.2007.03.775
Effect of atorvastatin therapy in the adiponectin levels in ananimal model of diabetes and hypercaloric dietPedroMonteiro, PauloMatafome,Marta Paiva, Raquel Carreira,Raquel Seiça, Lino Gonçalves, Luís A. Providencia. BasicResearch Unit in Cardiology, Cardiology Department andPhysiology Department, Coimbra Medical School, Coimbra,Portugal
Introduction: Obese diabetics havemore and worse ischemicheart disease. It was already demonstrated that diabetes (DM)induces changes in the levels of several adypokines and this canworsen the prognosis of these subjects. However, the impact ofDM in the context of a hypercaloric diet and its modulation by thechronic use of atorvastatin is not fully known.
Aim: To evaluate, in a model of DM and hypercaloric diet, ifchronic therapy with atorvastatin can modify serum levels ofadiponectin.
Materials and methods: Goto–Kakizaki (GK) diabetic rats(fed with a hypercaloric diet between 2 and 6 months) weredivided in 2 groups (n=10/group): A—GKHD (not submitted toany drug), B—GKHDA (fed with the same diet and treated withatorvastatin between 5 and 6 months of age). At 6 months of age,serum levels of adiponectin were determined using a non-com-petitive enzyme-linked imunossorbent assay (ELISA) technique.
Results: Adiponectin levels were significantly lower ingroup B, when compared with GKHD animals (3.3±0.2 versus5.2±0.3 μg/mL).
Conclusion: In diabetic animals fed with a hypercaloric diet,chronic therapy with atorvastatin induces a significant decreasein adiponectin levels.
Keywords: Diabetes mellitus; Nutrition; Inflammation
doi:10.1016/j.yjmcc.2007.03.776
Effect of chronic metformin therapy in the mitochondrialfunction in an ex-vivo animal model of diabetes andhypercaloric diet submitted to global myocardialischemia–reperfusionPedro Monteiro, Paulo Matafome, Marta Paiva, Raquel Carreira,Raquel Seiça, Lino Gonçalves, Luís A. Providencia. BasicResearchUnit in Cardiology, CardiologyDepartment and Physio-logy Department, Coimbra Medical School, Coimbra, Portugal
Aim: To evaluate, in a model of diabetes+hypercaloricdiet+ ischemia–reperfusion (IR), if chronic therapy with MET
improves cardiac mitochondrial function. Materials andmethods: Goto–Kakizaki (GK) diabetic rats (fed with anhypercaloric diet between 2 and 6 months) were divided in 4groups (n=10/group): A—GKHD control (no medication/noIR); B—MET control (Metformin 10 mg/kg/day betweenmonth 5 and 6/no IR); C—GKHD IR (as GKHD control andthen IR); D—MET IR (as MET control and then IR). At6 months, hearts were removed and submitted to 165 minperfusion (control) or 10 min perfusion +35 min ischemia+120 min reperfusion (IR). Mitochondrial parameters assessedwere: oxidative stress (colorimetric thiobarbituric acid colori-metry test—TBARS), mitochondrial swelling and calciumuptake (fluorimetry).
Results: MET-treated rats had significantly lower oxidativestress levels during IR (0.94±0.03 vs. 1.05±0.02 nmolTBARS/mg protein; p<0.05).MET-treated animals also showeda significant decrease in mitochondrial swelling in IR (57.7±2.3vs. 68.1±1.8 arbitrary units—AU; p<0.05). MET therapyshowed a trend towards an improvement in calcium uptake.
Conclusion: In our model, MET improves cardiac mito-chondrial function, due to less oxidative stress and betterischemia tolerance.
Keywords: Diabetes mellitus; Nutrition; Ischemia–reperfusion
doi:10.1016/j.yjmcc.2007.03.777
Impact of the chronic therapy with lipid lowering andantidiabetic drugs in the protein oxidative stress levels in ananimal model of diabetes treated with an hypercaloric dietPedroMonteiro, PauloMatafome,Marta Paiva, Raquel Carreira,Raquel Seiça, Lino Gonçalves, Luís A. Providencia. BasicResearch Unit in Cardiology, Cardiology Department andPhysiology Department, Coimbra Medical School, Coimbra,Portugal
Aim: To evaluate, in a model of DM fed with a hypercaloricdiet, if the chronic use of lipid-lowering and antidiabetic drugscan alter the protein oxidative stress levels.
Materials and methods: Goto–Kakizaki (GK) diabetic rats(fed with an hypercaloric diet between 2 and 6 months) weredivided in 6 groups (n=10/group): A—GKHD (not submittedto any drug), B—GKHD A (fed with the same diet and treatedwith atorvastatin between 5 and 6 months of age), C—GKHD I(fed with the same diet and treated with insulin between 5 and6 months of age), D—GKHD M (fed with the same diet andtreated with metformin between 5 and 6 months of age), E—GKHD G (fed with the same diet and treated with gliclazidebetween 5 and 6 months of age) and F—GKHD IA (fed with thesame diet and treated with insulin+atorvastatin between 5 and6 months of age). At 6 months, the level of carbonyl groupsformation (an indicator of protein oxidative stress) wasdetermined using a spectrophotometer.
Results: The level of carbonyl groups formation showed atrend towards being lower in all the animal groups submitted todrug therapy, when compared to the GKHD.
S60 ABSTRACTS / Journal of Molecular and Cellular Cardiology 42 (2007) S55–S71