نوع مقاله : مقاله پژوهشی
نویسندگان
1 دانشجوی دکتری فیزیولوژی ورزش، دانشکده فرهنگ و ارتباطات واحد کرج، دانشگاه آزاد اسلامی، کرج، ایران.
2 دانشیار، گروه فیزیولوژی ورزش، دانشکده فرهنگ و ارتباطات واحد کرج، دانشگاه آزاد اسلامی، کرج، ایران.
3 استادیار، گروه فیزیولوژی ورزش، دانشکده فرهنگ و ارتباطات واحد کرج، دانشگاه آزاد اسلامی، کرج، ایران.
چکیده
کلیدواژهها
عنوان مقاله [English]
نویسندگان [English]
Extended Abstract
Background and Aim: Non-alcoholic fatty liver disease (NAFLD) is an acquired metabolic disorder characterized by the accumulation of triglycerides in the liver, resulting from causes other than alcohol consumption. Exercise has been shown to not only reduce liver inflammation but also enhances mitochondrial biogenesis, improving morphological dynamics and regeneration rates through biogenesis and mitophagy. In addition , insect-based supplements, such as mealworms, have demonstrated strong immunostimulatory, anticancer, antidiabetic, and antioxidant properties. This supplement, rich in protein, has been reported to exhibit anti-obesity effects by activating peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). Furthermore, it has been shown to effectively reduce weight and fat mass by influencing the expression of genes involved in fat metabolism. Therefore, the present study aimed to investigate the combined effect of mealworm protein supplementation and aerobic exercise on the expression of genes associated with mitochondrial biogenesis—including PGC-1α, uncoupling protein 1 (UCP1), mitofusin 1 (Mfn1), and dynamin-related protein 1 (Drp1)—in the soleus muscle tissue of rats with NAFLD.
Materials and Methods: In this experimental study, 25 male Wistar rats were divided into five equal groups including: 1- healthy, 2- patient, 3- patient+supplement, 4- patient+exercise, 5- patient+supplement+exercise. The sick groups developed NAFLD with high fat and cholesterol diet. The exercise protocol consisted of interval endurance exercise was performed for eight weeks, involving treadmill running for 30 minutes per session, five days per week with gradual overload. Mealworm protein supplement was administered via oral gavage at a dose of 20 mg/kg body weight on the same days as exercise sessions.
Tissue sampling of the soleus muscle was performed 48 hours after the last exercise and supplement session. The animals were anesthetized with intraperitoneal injections of Ketamine and Xylazine, and the soleus muscle tissue was immediately collected. Each tissue sample was placed in a microtube containing liquid nitrogen and stored at -80°C until gene expression analysis.
Total RNA was extracted using the RNX-Plus method, and RNA purity and concentration were determined by spectrophotometry and confirmed by Agarose gel electrophoresis. The mRNA sequences of target genes (PGC-1α, UCP1, Mfn1, and Drp1) were obtained from the NCBI database. Primer sequences were designed using AllelID software and validated for specificity using BLAST analysis.
Data were analyzed using independent t-tests and two-way ANOVA, with the significance level set at p≤ 0.05.
Results: The independent t-test results revealed that in the diseased group, the expression of PGC-1α, UCP1, and Mfn1 genes significantly decreased compared to the healthy group, while the expression of Drp1 significantly increased (p=0.0001). According to the two-way ANOVA (Table 1) and Bonferroni tests, aerobic exercise significantly increased the expression of PGC-1α (p=0.0001), UCP1 (p=0.0001), and Mfn1 (p=0.0001), while significantly decreased the expression of Drp1 (p=0.0001) in the soleus muscle tissue of rats with NAFLD. Additionally, statistical findings revealed that mealworm protein supplementation significantly increased the expression of UCP1 (p=0.0001), PGC-1α (p=0.0001), and Mfn1 (p=0.0001), while significantly decreased the expression of Drp1 (p=0.0001) in the soleus muscle tissue of rats with NAFLD. However, the two-way ANOVA (Table 1) and Bonferroni tests, showed that the combination of aerobic exercise and mealworm protein supplementation did not have a significant effect on the expression of UCP1 (p=0.53), PGC-1α (p=0.36), or Drp1 (p=0.88) in the soleus muscle tissue of rats with NAFLD. Nevertheless, the simultaneous intervention of aerobic exercise and mealworm protein supplementation significantly increased the expression of Mfn1 (p=0.0001) in the soleus muscle tissue of rats with NAFLD.
Conclusion: The findings of this study demonstrate that both intermittent aerobic exercise and mealworm protein supplementation independently led to a significant upregulation of key genes involved in mitochondrial biogenesis—namely PGC-1α, UCP1, and Mfn1—in the soleus muscle of rats with NAFLD. Concurrently, these interventions resulted in a marked downregulation of Drp1, a gene associated with excessive mitochondrial fission and cellular apoptosis. These gene expression changes reflect improved mitochondrial function, enhanced fatty acid oxidation capacity, and reduced oxidative stress in muscle tissue—all of which are critical factors in the management and potential reversal of NAFLD. Notably, the interaction effect between exercise and supplementation was significant only for Mfn1 expression, suggesting a synergistic role in promoting mitochondrial fusion and stabilizing mitochondrial membrane potential. This may contribute to reduced apoptosis and improved mitochondrial dynamics under pathological conditions. Given the pivotal roles of the investigated genes in lipid metabolism, metabolic flexibility, and cellular homeostasis, the results suggest that both aerobic exercise and mealworm protein supplementation represent promising non-pharmacological strategies for mitigating NAFLD. Furthermore, considering the antioxidant, anti-obesity, and metabolic regulatory properties of mealworm supplementation, along with the well-established benefits of aerobic exercise in enhancing mitochondrial performance and reducing inflammation, the combination of these two interventions may offer a novel and multifaceted therapeutic approach for metabolic disorders such as NAFLD. However, further research is recommended—particularly in advanced animal models and clinical trials involving individuals with obesity or type 2 diabetes who are at risk for NAFLD.
Hical Considerations: Ethical approval was obtained from the Ethics Committee of Islamic Azad University, Karaj Branch (Code: IR.IAU.K.REC.1403.029).
Funding: The costs of the study were borne by the researcher.
Conflict of Interest: No conflicts of interest declared.
کلیدواژهها [English]
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