Changes in expression of genes related to glucose metabolism in liver and skeletal muscle of rats exposed to acute hypoxia

Yurie Hara,Nakamichi Watanabe

doi:10.1016/j.heliyon.2020.e04334

Abstract

The aim of this study was to determine changes in gene expression associated with glucose metabolism in the liver and soleus muscles of rats exposed to hypoxia to improve work capacity under high altitude conditions. Rats were divided into normobaric normoxia (control) and normobaric hypoxia (hypoxia) groups (n = 7 each), and the hypoxia group was exposed to 10.5% oxygen for 90 min. Glucose metabolism-related gene expression was examined by real-time polymerase chain reaction. In the liver, the expression levels of the glucose utilization-related genes solute carrier family 2 member 1, glucokinase, and liver-type phosphofructokinase and the gluconeogenesis-related gene phosphoenolpyruvate carboxykinase 1 (Pck1) were significantly increased upon hypoxic exposure. In contrast, gene expression in the soleus was unchanged, with the exception of Pck1. The results suggest that under hypoxia, both glucose utilization and gluconeogenesis are accelerated in the liver, and liver glycogen is degraded to maintain blood glucose level.

Highlights

Hypoxic conditions, such as high altitudes and strenuous exercise, induce metabolic changes [1]
The aim of this study was to examine changes in the expression of genes related to glucose metabolism in the liver and soleus muscle of rats exposed to normobaric hypoxia, to identify organs with accelerated glucose utilization in this condition and assess changes in liver glycogen content
This study suggests that hypoxic exposure enhances the expression of genes related to glucose uptake (Slc2a1) and glycolysis (Gck and Pfkl) in the liver, while glucose metabolism-related gene expression in the soleus muscle was not affected

Summary

Introduction

Hypoxic conditions, such as high altitudes and strenuous exercise, induce metabolic changes [1]. Hypoxic exposure reduces liver glycogen contents in rats and mice [3, 5, 6, 7, 8]. These metabolic changes, i.e., the acceleration of glucose utilization and the depletion of liver glycogen, induce hypoglycemia, which can result in decreased work capacity due to increased fatigue [9, 10]. Hypoxic exposure has been shown to increase glycogen accumulation induced by glycogen synthase activation in myoblasts, ovarian clear cell carcinoma, and cultured rat heart muscle [11, 12, 13]

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