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ISSN (Print): 2666-8629
ISSN (Online): 2666-8637

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Research Article

Curcumin Modulates the Expression of PPARα, CPT1, and MCAD to Prevent Lipid Metabolism Alterations in the Hearts of Mice Fed with an HFD

Author(s): Cecilia G. Meléndez-Salcido, Katya Vargas-Ortiz, Oscar G. Silva-Gaona, María C. León-García, Maciste H. Macías-Cervantes, Joel Ramírez-Emiliano and Victoriano Pérez-Vázquez*

Volume 1, Issue 1, 2023

Published on: 23 August, 2022

Article ID: e260422204055 Pages: 7

DOI: 10.2174/2666862901666220426103916

Price: $65

Abstract

Background: Consuming 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 cardiometabolic diseases, although it has not been demonstrated.

Objective: This article evaluates the effect of curcumin on the expression of the PPARα, CPT1, MCAD, VLCAD, and ACAA2 genes in the hearts of mice fed with an HFD.

Methods: Four groups of male C57BL/6 mice (n = 6) were treated for 15 weeks as follows: 1) standard diet (C), 2) standard diet + 0.75% (w/w) curcumin (C+Cur), 3) standard diet + 30% (w/v) fructose (F), and 4) standard diet + 0.75% (w/w) curcumin + 30% (w/v) fructose (F+Cur). Bodyweight gain, glucose, and the overall serum cholesterol levels were measured after the 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 an HFD. However, it did not affect VLCAD expression.

Conclusion: Curcumin regulated 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 an HFD.

Keywords: Cardiovascular disease, curcuma longa, high-fructose diet, lipid metabolism, mitochondrial metabolism, obesity.

Graphical Abstract

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