Aim: High-fructose intake induces nonalcoholic fatty liver disease (NAFLD) and chronic intermittent hypobaric hypoxia (CIHH) has beneficial effects on the body. We hypothesized that CIHH has protective effects on the impaired hepar in fructose-fed rats.
Main methods: Sprague-Dawley rats (male, 160-180 g) were randomly divided into 4 groups: control group (CON), fructose group (FRUC, 10% fructose in drinking water for 6 weeks), CIHH group (simulated 5000m altitude, 6h per day for 6 weeks), and CIHH plus fructose groups (CIHH-F). Histopathology of liver, arterial blood pressure, blood biochemicals, hepatocyte apoptosis, and marker proteins of endoplasmic reticulum stress (ERS) were measured.
Key findings: The arterial blood pressure, body mass index, abdominal fat weight and liver weight were increased in FRUC rats but not in CIHH-F rats. Likewise, the serum glucose, insulin, insulin C peptide, triglyceride (TG) and total cholesterol (TC) were elevated in FRUC rats but not in CIHH-F rats after fasting 12h. Meanwhile, the hepatic steatosis and hepatocyte apoptosis occurred in FRUC rats but not in CIHH-F rats. Finally the expression of ERS markers including GRP78 (glucose-regulated protein78), CHOP (C/EBP Homologous Protein), and caspase-12 in hepatic tissue were up-regulated in FRUC rats, but such up-regulation was not observed in CIHH-F rats.
Significance: Our results suggest that CIHH protect hepar against hepatic damage through inhibition of ERS in fructose-fed rats. CIHH might be the new therapy for NAFLD.
Keywords: Apoptosis; Chronic intermittent hypobaric hypoxia; Endoplasmic reticulum stress; Fructose (PubChem CID: 5984); Hepar; Metabolic syndrome.
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