The hepatic protection effects of hepassocin in hyperglycemic crisis

Horng Yih Ou, Hung Tsung Wu, Ching Han Lin, Ye Fong Du, Che Yuan Hu, Hao Chang Hung, Pansee Wu, Hung Yuan Li, Shu Huei Wang, Chih Jen Chang

研究成果: Article同行評審

22 引文 斯高帕斯(Scopus)


Context: High glucose generates reactive oxygen species (ROS) and contributes to glucotoxicity in hepatocytes, and hyperglycemia causes structural and functional damage to the liver. However, only a mild hepatic dysfunction was observed in subjects with hyperglycemic crisis, implying a factor exists to exert a hepatic protective effect. Hepassocin is a hepatokine that modulates the proliferation and metabolism of hepatocytes and also exerts protective activity in liver injury. However, its role in hyperglycemic crisis-induced hepatic dysfunction remains unknown. Objective: To investigate the possible hepatic protection effects of hepassocin in hyperglycemic crisis. Design, Setting, and Patients: Plasma hepassocin concentrations and routine biochemistry were measured in 21 patients with hyperglycemic crisis before and after standard treatments. The effects of hepassocin on hepatic functions were evaluated in streptozotocin-induced hyperglycemic mice (STZ mice). HepG2 cells were used to clarify the possible mechanisms regulating hepassocin expression. Results: Plasma hepassocin concentrations decreased significantly in subjects with hyperglycemic crisis after standard treatment accompanied by improved hepatic functions. Correction of hyperglycemia in STZ mice also decreased the hepatic hepassocin expression. Injection of recombinant hepassocin improved hepatic functions and histologic changes and increased the expression of antioxidative stress proteins, including superoxide dismutase 1 (SOD1). In HepG2 cells, high glucose increased hepassocin expression through signal transducer and activator of transcription 3 and hepatocyte nuclear factor-related pathways. We also demonstrated that hepassocin increased SOD1 expression through an extracellular signal-regulated kinase 1/2 nuclear factor erythroid-2-related factor 2 pathway, decreasing ethyl acetate-induced ROS production and improving cell viability. Conclusions: Increased hepassocin secretion in hyperglycemic crisis might offset the deleterious effects of hyperglycemia on hepatocytes.

頁(從 - 到)2407-2415
期刊Journal of Clinical Endocrinology and Metabolism
出版狀態Published - 2017 7月 1

All Science Journal Classification (ASJC) codes

  • 內分泌學、糖尿病和代謝
  • 生物化學
  • 內分泌
  • 臨床生物化學
  • 生物化學(醫學)


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