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Hamzeh Bayani, Habib Asgharpour, Asra Askari, Reza Rezaeeshirazi,
Volume 10, Issue 3 (10-2022)
Abstract

Background and Objective: Regular exercise along with calorie intake promotes mitochondrial function by promoting healthy mitochondrial regeneration. The aim of the present study was to investigate the effect of four weeksof continuous aerobic training and starvation on the gene expression of pink1 and bnibp3 (liver mitophagy) in Wistar fat rats.
Materials and Methods: The present study used an experimental design. Thirty 18-week-old fatty, maleWistar rats with an average body weight of 348±25.53 purchased from the Pasteur Institute of Iran were selected as the research sample. After one week of familiarity with the laboratory environment, these fatty animals were randomly divided into 6 groups of 5, control (n=5) and experimental (n=25), including control, starvation, starvation and 3 days of exercise, starvation and 5 days of exercise, 3 days of exercise, 5 days of exercise groups.
Results: According to the statistical results of one-way analysis of variance, there was a significant decrease in triglyceride, cholesterol, liver enzymes ALT, AST in all groups compared to the control group. Furthermore, there was a significant increase in pink1 and bnibp3 gene expression in starvation group and starvation groups of 3 and 5 days of training compared to the control group.
Conclusion: Four weeksof continuous aerobic training and starvation combined and alone were able to significantly reduce the status of blood lipids and liver enzymes in fatty model rats. Also, the starvation group and starvation groups along with exercise increased the activity of removing damaged mitochondria by increasing the activity of pink1 and bnibp3 genes compared to the control group.
 

Jahanbakhsh Asadi , Asra Askari , Zeinab Mohammadi , Babaisan Askari ,
Volume 13, Issue 2 (6-2025)
Abstract

Background: The higher occurrence of NAFLD is associated with insulin resistance, obesity, and diabetes. A diet with high fat or sucrose serves as a NAFLD inducer in rats, which exhibits significant variability and generally results in low levels of liver inflammation and fibrosis. Our study highlights the role of combining animal fats with high sucrose in inducing NAFLD in Wistar rats.
Methods: Twenty male Wistar rats, 8 to 10 weeks old, were randomly divided into two groups: Control (healthy) and NAFLD induction. Weekly weight changes were recorded. After one week of adapted feeding, a 30% vegetable oil and 10% solid sugar diet was added to standard pellets to induce the NAFLD model. After ten weeks, the weight/time of progression of each mouse was measured. Serum and tissue samples were separated and stored for biochemical and histopathological studies. Comparisons were made using independent t-test for two groups with SPSS version 22. The significance level was set at 0.05.
Results: Our results illustrated that weight/time progress increased in the NAFLD-induced group (0.679 g ± 0.02, P < 0.001) more than in the control group (0.559 g ± 0.03). Additionally, FBS (P = 0.001), lipid profile [TG/HDL (P = 0.006), LDL/HDL (P = 0.03), Chol/HDL (P = 0.006), TG (P = 0.005), CHOL (P = 0.001), LDL (P = 0.008), VLDL (P = 0.005), HDL (P = 0.01)], liver function enzymes [ALT (P = 0.001), AST (P = 0.001)[ and IL-6 serum levels were significantly increased in the NAFLD-induced group compared to control rats (P = 0.001). Besides, the obtained results illustrated that the serum level of albumin was significantly decreased in NAFLD-induced rats compared to controls (P = 0.004). Moreover, Oil Red and H&E staining confirmed grade two steatosis induction.
Conclusion: Our study demonstrates significant metabolic abnormalities and steatosis in NAFLD-induced rats, underscoring the detrimental impact of this disease on liver function and overall health. These findings highlight the urgent need for further research into effective interventions for NAFLD.
 


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