Abstract

This study examined the effects of defatted mealworm fermentation extract (MWF) on alcoholic liver injury in rats. The rats were fed either a Lieber-DeCarli control (Con) or alcohol liquid diet (EtOH). The alcohol-fed rats were administered MWF (50, 100, or 200 mg/kg/day) and silymarin (200 mg/kg/day) orally for eight weeks. MWF prevented alcohol-induced hepatocellular damage by decreasing their serum aspartate transaminase, alanine transaminase, and gamma-glutamyl transpeptidase levels significantly compared to the EtOH group. MWF effectively reduced the relative hepatic weight, lipid contents, and fat deposition, along with the down-regulation of transcriptional factors and genes involved in lipogenesis compared to the EtOH group. It also enhanced the antioxidant defense system by elevating the glutathione level and glutathione reductase activity. MWF attenuated the alcohol-induced inflammatory response by down-regulating hepatic inflammation-associated proteins expression, such as phosphorylated-inhibitor of nuclear factor-kappa B-alpha and tumor necrosis factor-alpha, in chronic alcohol-fed rats. Furthermore, sequencing analysis in the colonic microbiota showed that MWF tended to increase Lactobacillus johnsonii reduced by chronic alcohol consumption. These findings suggest that MWF can attenuate alcoholic liver injury by regulating the lipogenic and inflammatory pathway and antioxidant defense system, as well as by partially altering the microbial composition.

Highlights

  • Alcohol metabolism has numerous detrimental consequences, including the formation of acetaldehyde adducts and reactive oxygen species (ROS)

  • hematoxylin and eosin (H&E) staining data showed that mealworm fermentation extract (MWF) (50, 100, and 200 mg/kg) and silymarin (200 mg/kg) reduced hepatic fat globules and focal necrosis compared with the EtOH group (Figure 1A)

  • The indirect effects of MFW on liver might be mediated by alterations of gut microbiota, which will be further elucidated in future works

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Summary

Introduction

Alcohol metabolism has numerous detrimental consequences, including the formation of acetaldehyde adducts and reactive oxygen species (ROS). It changes the ratio of the reduction and oxidation state of hepatocytes that contribute to the tissue damage and diseases observed in alcoholic patients [1]. The initiation and progression of alcoholic liver disease (ALD). Hepatic steatosis is an initial manifestation of ALD in response to excess alcohol. Pharmacological treatments to improve ALD are still limited because of the side effects of synthetic medicines with hepatic protective activity. Stable and safe therapeutic strategies are needed to improve the progression of ALD for patients who do not stop drinking [5]

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