Background: It has been proposed that curcumin modulates the gene expression of different signaling pathways, improve the fatty acids metabolism and exerts a potential beneficial effect on cardiometabolic disease, but this has not been thoroughly demonstrated. In the present study, we evaluated the effect of curcumin upon the expression of PPARα, CPT1, MCAD, VLCAD and ACAA2 in heart of mice fed a high-fructose diet (HFD).Methods: Twenty-four mice C57BL/6 were divided into four groups (n=6) and treated for 15 weeks. Control group (C) received standard diet (SD), Curcumin group (C+Cur), Fructose group (F) and Fructose with Curcumin group (F+Cur). The groups were treated with 0.75% w/w curcumin mixed in the SD and 30% w/v fructose in water, respectively. Heart proteins expression were analyzed by Western Blot.Results: Curcumin supplementation increased PPARα and ACAA2 expression and decreased CPT1 and MCAD expression in heart of mice fed a HFD. However, it did not modify the VLCAD expression.Conclusions: Curcumin regulated PPARα, CPT1 and MCAD expression and increased ACAA2 expression; suggesting a therapeutic potential in the prevention of alterations in mitochondrial fatty acids metabolism in heart of mice fed a HFD.
Background: A high fructose diet (HFD) induces protein glycation. The latter is related to a higher risk of cardiovascular disease. Curcumin is a natural pleiotropic compound that may possess antiglycant properties. Objective: To analyze the effect of curcumin on the content of glycated proteins in the hearts of 6-week-old mice fed with a HFD for 15 weeks. Methods: Mice were allocated in four groups (n = 6/group): a control group that received a standard diet (CT); a group that received 30% w/v fructose in water (F); a group that received 0.75% w/w curcumin supplemented in food (C); a group that received 30% w/v fructose in water and 0.75% w/w curcumin supplemented in food (F+C). The content of glycated proteins in the heart was determined by Western Blot (whereas the spots were detected by 2D-PAGE) using anti-AGE and anti-CML antibodies. A densitometric analysis was performed using the ImageLab software. Glycated proteins were identified by MALDI-TOF-MS, and an ontological analysis was performed in terms of biological processes and molecular function based on the STRING and DAVID databases. Results: Fourteen glycated protein spots were detected, two of them with anti-AGE and the other 12 with anti-CML. In total, eleven glycated proteins were identified, out of which three had decreased glycation levels due to curcumin exposure. The identified proteins participate in processes such as cellular respiration, oxidative phosphorylation, lipid metabolism, carbohydrate metabolism, the tricarboxylic acid cycle (TAC), and the organization of intermediate filaments. Conclusions: Curcumin decreased the fructose-induced glycation level of the ACO2, NDUFS7, and DLAT proteins.
Background: In type 2 diabetic mouse liver, hyperglycemia, and insulin modify gene expression. Curcumin is a powerful antioxidant and antidiabetic agent that regulates the gene expression of different signaling pathways through various transcription factors. Therefore, we hypothesized that curcumin modifies the protein expression profile in the liver of diabetic db/db mice. Objective: To determine the effects of curcumin on the liver protein profile of diabetic db/db mice. Methods: db/db and wild type (WT) male mice were allocated in four groups, and they were fed for eight weeks. Three WT and three diabetic db/db mice received a standard diet (SD; WT and db/db groups, respectively); three WT and three diabetic db/db mice received a SD supplemented with 0.75 % (w/w) curcumin (WT+C and db/db+C groups, respectively). Liver proteins were separated by 2D electrophoresis. Differential protein expression analysis was performed on ImageMaster 2D Platinum software, and selected proteins were identified by MALDI-TOF-MS and subjected to enrichment analysis using STRING and DAVID databases. Results: Thirty-six proteins with differential expression due to the diabetic background and curcumin treatment were found; these proteins participate in the metabolism of amino acids, carbohydrates, and lipids. Interestingly, the altered expression of seven proteins was prevented in the liver of the diabetic mice that received curcumin. Conclusions: Among all differentially expressed proteins, curcumin reverted the altered expression of seven proteins. Thus, although it was observed that curcumin did not affect the biochemical parameters, it does modify the expression of some liver proteins in diabetic mice.
Background: the consumption of a high-fructose diet (HFD) contributes to obesity, dyslipidemia, and cardiovascular diseases. It has been proposed that curcumin modulates lipid metabolism and it has a potential beneficial effect in the context of the cardiometabolic diseases, although it has not been clearly demonstrated Objective: to evaluate the effect of curcumin on the expression of the PPARα, CPT1, MCAD, VLCAD, and ACAA2 genes in the hearts of mice fed with a HFD. k (F), and 4) standard diet + 0.75% (w/w) curcumin + 30% (w/v) fructose (F+Cur). The gain of body weight, glucose, and the overall serum cholesterol levels were measured after the respective treatment. The expression of PPARα, MCAD, VLCAD, ACAA2, and CPT1 was assessed by Western blot in mice hearts. Results: our data showed that a curcumin treatment induced a higher expression of PPARα and ACAA2 whereas it decreased CPT1 and MCAD expression in the hearts of mice fed with a HFD. However, it had no effect on VLCAD expression Conclusion: curcumin regulates PPARα, CPT1, and MCAD expression and increased that of ACAA2. This suggests a possible therapeutic use to prevent the alterations of mitochondrial fatty acid metabolism in the hearts of mice fed with a HFD.
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