High-Fructose Diet-Induced Metabolic Disorders Were Counteracted by the Intake of Fruit and Leaves of Sweet Cherry in Wistar Rats - PubMed (original) (raw)

High-Fructose Diet-Induced Metabolic Disorders Were Counteracted by the Intake of Fruit and Leaves of Sweet Cherry in Wistar Rats

Kinga Dziadek et al. Nutrients. 2019.

Abstract

Numerous studies have indicated that the use of plants rich in bioactive compounds may reduce the risk of non-communicable diseases. The aim of this study was to investigate how the addition of fruit and leaves to high-fructose diet affects lipid metabolism, including the expression of genes involved in fatty acid synthesis and oxidation in the liver and adipose tissue, as well as oxidative stress and inflammation in Wistar rats. The animals were fed with AIN-93G diet, high fructose (HFr) diet, HFr diet with addition of 5% or 10% freeze-dried fruits, and HFr diet with addition of 1% or 3% freeze-dried leaves. The experiment lasted 12 weeks. The results showed that the intake of fruit and leaves of sweet cherry caused the improvement of the liver function, as well as beneficially affected lipid metabolism, among others, by regulating the expression of genes associated with fatty acid synthesis and β-oxidation. Additionally, they exhibited antioxidant and anti-inflammatory properties. In conclusion, the addition of fruit and leaves reduced the adverse changes arising from the consumption of high fructose diet. Therefore, not only commonly consumed fruits, but also leaves can be potentially used as functional foods. These findings may be helpful in prevention and treatment of the obesity-related metabolic diseases, especially cardiovascular diseases.

Keywords: Wistar rats; antioxidant enzymes; high fructose diet; inflammation; lipid metabolism genes; sweet cherry leaves.

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Conflict of interest statement

The authors declare that there are no conflicts of interest.

Figures

Figure 1

Figure 1

The expression of fatty acid synthesis genes (Fasn, Acaca, Scd1, Mlxipl and Srebf1) and fatty acid oxidation genes (Cpt1a and Ppar-α) in liver of rats. NC—negative control; HFr—high fructose; HFr + F5%—HFr diet with addition of 5% of fruits; HFr + F10%—HFr diet with addition of 10% of fruits; HFr + L1%—HFr diet with addition of 1% of leaves; HFr + L3%—HFr diet with addition of 3% of leaves. Data are expressed as mean ± SD. Values with different letters (a–f) are statistically different (p < 0.05).

Figure 2

Figure 2

The expression of fatty acid synthesis genes (Fasn, Acaca, Scd1, Mlxipl) in adipose tissue of rats. NC—negative control; HFr—high fructose; HFr + F5%—HFr diet with addition of 5% of fruits; HFr + F10%—HFr diet with addition of 10% of fruits; HFr + L1%—HFr diet with addition of 1% of leaves; HFr + L3%—HFr diet with addition of 3% of leaves. Data are expressed as mean ± SD. Values with different letters (a–d) are statistically different (p < 0.05).

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