Effect of hepatic sympathetic nerve removal on energy metabolism in an animal model of cognitive impairment and its relationship to Glut2 expression

Author:

Wei Riming1,Zhuge Xiuhong2,Yue Pengpeng1,Liu Manjun2,Zhu Lin2,Liu Jianxiang1,Xia Chunbo3

Affiliation:

1. College of Biotechnology, Guilin Medical University, Guilin, Guangxi, 541004, China

2. Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, 541004, China

3. Department of Human Anatomy of Basic Medical College, Guilin Medical University, Guilin, Guangxi, 541004, China

Abstract

AbstractThe aims of this study were to investigate the effect of hepatic sympathetic nerve removal on glucose and lipid metabolism in rats with cognitive impairment and to evaluate the relationship between these effects and liver Glut2 expression. Hippocampal injection of Aβ1–42 was used to induce cognitive impairment. Impaired rats were divided into experimental, sham, and control groups. The experimental group was injected with 6-hydroxydopamine to remove the sympathetic nerve. At 4 weeks post injection, body weight, food and water intake, blood sugar, and blood lipids were measured, and periodic acid-Schiff (PAS) staining was used to assess the liver glycogen content. Liver Glut2 mRNA and protein were also detected. The experimental group showed reduced body weight, food intake, and blood glucose levels and elevated insulin levels compared with the control group. PAS staining showed higher glycogen contents in the experimental group than in controls. The expression levels of Glut2 mRNA and protein in the experimental group were significantly lower than in the controls. Metabolism was significantly impacted in rats with cognitive impairment following removal of the hepatic sympathetic nerve. Disruption to Glut2 liver expression via sympathetic nerve disruption represents a possible underlying mechanism.

Publisher

Walter de Gruyter GmbH

Subject

General Agricultural and Biological Sciences,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Neuroscience

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