Investigation of the Repairing Effect and Mechanism of Oral Degraded Sericin on Liver Injury in Type II Diabetic Rats.

Zhen-Zhen Wei,Yu-Qing Zhang,Yu-Jie Weng

doi:10.3390/biom12030444

Abstract

In the sericulture and silk production industry, sericin is discharged in the degumming wastewater, resulting in a large amount of wasted natural protein and environmental pollution. This study investigated the effect of degraded sericin recovered by the Ca(OH)2–ultrasound degumming method (a green process) on liver injury in T2D rats. After 4 weeks of dietary sericin supplementation, the liver masses and organ coefficients of the T2D rats improved compared with those of the model rats that were not fed sericin. Oral sericin activated the damaged PI3K/AKT/AMPK pathway to enhance glycogen synthesis, accelerate glycolysis, and inhibit gluconeogenesis. The protein expression levels of the inflammatory factors NF-κB, IL-6, and TNF-α in the T2D model group were up to two times higher than in the normal group. However, all three T2D groups that received oral sericin showed significant decreases in these factors to the level found in the normal group, indicating that inflammation in the body was significantly reduced. These results show that the sericin protein might improve glycogen synthesis, accelerate glycolysis, and inhibit gluconeogenesis by enhancing the anti-oxidation capability and reducing inflammatory reactions. Therefore, sericin recovered by Ca(OH)2 degradation has potential use in the development of functional health foods that can lower blood sugar.

Highlights

The classic symptom of diabetes is insulin resistance, a primary cause of oxidative stress [1,2], which is reflected in increased levels of reactive oxygen species (ROS) in the liver
Studies have found that it can be an important part of the treatment of diabetes, cancer, neurodegenerative diseases, and stroke targeting; AMPK (AMP-dependent protein kinase) is an important sensor molecule that regulates bioenergy homeostasis, which can control the synthesis and decomposition pathways of energy metabolism
We explored the ability of sericin to repair liver damage and its mechanism of action in diabetic rats in terms of glucose and lipid metabolism, the PI3K/AKT signaling pathway, and the AMPK/Acetyl-CoA carboxylase (ACC)

Summary

Introduction

Das. The classic symptom of diabetes is insulin resistance, a primary cause of oxidative stress [1,2], which is reflected in increased levels of reactive oxygen species (ROS) in the liver. The liver is the most important target organ of insulin [3]. Activated PI3K generates a second messenger and promotes the activation of AKT (protein kinase B). The insulin/PI3K/AKT pathway plays an important role in regulating liver carbohydrate metabolism. Studies have found that it can be an important part of the treatment of diabetes, cancer, neurodegenerative diseases, and stroke targeting; AMPK (AMP-dependent protein kinase) is an important sensor molecule that regulates bioenergy homeostasis, which can control the synthesis and decomposition pathways of energy metabolism. The liver is the main organ that regulates blood sugar levels

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Conclusion