Protective effect of protein hydrolysates from Litopenaeus vannamei waste on oxidative status, glucose regulation, and autophagy genes in non-alcoholic fatty liver disease in Wistar rats

Iran J Basic Med Sci. 2022 Aug;25(8):954-963. doi: 10.22038/IJBMS.2022.62167.13761.

Abstract

Objectives: The effects of protein hydrolysates (FP) from Litopenaeus vannamei on oxidative stress, and autophagy gene expression was investigated in the NAFLD-induced rats.

Materials and methods: For this purpose, twenty-four male rats were divided into four groups: Control, High-fat diet (HFD), FP20+HFD, and FP300+HFD (20 and 300 mg FP /kg rat body weight) and fed for 70 days.

Results: The results indicated that the rat body and relative weight of the liver were not affected by experimental treatments (P>0.05) although the highest relative weight of the liver was observed in HFD treatment. The highest and lowest values for antioxidant enzymes and MDA concentration were observed in FP treatments (P<0.05). Also, the results showed that FP significantly decreased liver enzymes (ALT, AST) in the liver in comparison with HFD treatment (P<0.05). Plasma biochemical indices were investigated and the lowest amylase, ALP, fasting glucose, insulin, HOMA-IR, triglycerides, cholesterol, and inflammation cytokines (TNF-α, IL-6) were seen in the FP treatments which had a significant difference with HFD (P<0.05). Autophagy gene expression in the liver cells was affected by experimental diets and the lowest expression of Beclin-1 and Atg7 was observed in HFD and FP300 treatments. Interestingly, the highest expression of LC3-ɪ and P62 was seen in HFD and FP treatments, not in the control.

Conclusion: Overall, the results of this experiment indicated that FPs extracted from Whiteleg shrimp at 50 °C improve the oxidative status, glucose metabolism, and autophagy gene expression and could be used as a useful nutritional strategy in fatty liver prevention.

Keywords: Autophagy; Bioactive peptides; Fatty liver; Insulin; Oxidative enzymes; Whiteleg shrimp.