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.
Scope
Obesity is a global threat for male infertility, which can cause spermatogenic dysfunction. However, there are no available drugs for the treatment of obesity‐induced spermatogenesis dysfunction. This study characterizes the protective effects of icariin (ICA) on spermatogenesis dysfunction in obese mice.
Methods and results
Obese mice are induced by a high‐fat diet to determine whether ICA has a protective effect. ICA treatment reduces body weight and the proportion of abnormal sperm, brings about a recovery of sperm count, and the number of spermatogenic cells. ICA treatment improves histopathological changes of the testes and inhibits testicular apoptosis, as evidenced by reduced the expression of Bax and increased the expression of Bcl‐2, PCNA, WT1, GATA‐4, vimentin, HK2, PKM2, and LDHA in the testes. In vitro, TM4 cells are treated with 0.4 mm palmitic acid (PA) to induce Sertoli cell injury, and are then utilized for ICA treatment. ICA improves PA‐induced decreased TM4 cells viability, reduces the levels of lactate, and increases the levels of pyruvate and the expression of HK2, PKM2, and LDHA and restores the glycolytic process in vitro.
Conclusion
ICA ameliorates spermatogenic dysfunction in obese mice by regulating glycolytic activity, providing effective strategies for obesity treatment.
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