Abstract

This study was performed to assess the effect of chronic intermittent hypoxia (CIH) on the liver, the associated mechanisms and the potential therapeutic roles of adiponectin (Ad). Sixty rats were randomly assigned to four groups: the normal control (NC), NC and Ad supplement (NC + Ad), CIH, and CIH and Ad supplement (CIH + Ad) groups. The rats in the CIH and CIH + Ad groups were exposed to a hypoxic environment for 4 months. Rats in the NC + Ad and CIH + Ad groups were also treated with an intravenous injection of Ad (10 ug), twice a week. The plasma levels of hepatic enzymes, serum triglyceride, liver triglyceride, fasting blood glucose and hepatic cell apoptosis in hepatic tissue, were higher in the CIH group than in the NC and NC + Ad groups. However, the Ad supplementation in the CIH + Ad group rescued the hepatic tissue insult by activating the AMP-activated protein kinase (AMPK) pathway. In conclusion, Ad could protect against CIH-induced hepatic injury partly through the AMPK pathway.

Highlights

  • This study was performed to assess the effect of chronic intermittent hypoxia (CIH) on the liver, the associated mechanisms and the potential therapeutic roles of adiponectin (Ad)

  • The liver triglyceride and the serum levels of ALT, AST, lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and triglyceride were higher in the CIH group than in the normal control (NC) and NC and Ad supplement (NC +Ad) groups, whereas those in the CIH and Ad supplement (CIH +Ad) group were significantly lower than those in the CIH group and higher than those in the NC and NC +Ad groups (Table 1)

  • We found that CIH could increase the liver lipid and triglyceride, fasting blood glucose (FBG) and the serum levels of AST, ALT and LDH, ALP and triglyceride, reduce the fasting insulin (FSI), and induce hepatic cell apoptosis

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Summary

Introduction

This study was performed to assess the effect of chronic intermittent hypoxia (CIH) on the liver, the associated mechanisms and the potential therapeutic roles of adiponectin (Ad). OSAS is associated with an increased risk of non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and fibrosis[8]. ER stress plays an important role in NAFLD in humans liver[16] and the liver transplantation in rats[17]. Adiponectin (Ad), an adipokine synthesized and excreted into the blood by adipose tissue, plays an important role in energy metabolism and adipocyte differentiation[20,21,22]. The aim of this study was to assess the effect of CIH alone on the liver and the protective roles of Ad as well as to uncover the underlying mechanisms

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