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: 雜誌貢獻文章

1 引文 (Scopus)

摘要

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.
原文英語
頁(從 - 到)2407-2415
頁數9
期刊Journal of Clinical Endocrinology and Metabolism
102
發行號7
DOIs
出版狀態已發佈 - 七月 1 2017
對外發佈Yes

指紋

Streptozocin
Liver
Superoxide Dismutase
Reactive Oxygen Species
Hepatocyte Nuclear Factors
Plasmas
Glucose
STAT3 Transcription Factor
Biochemistry
Mitogen-Activated Protein Kinase 3
Heat-Shock Proteins
Metabolism
Hyperglycemia
Hepatocytes
Obese Mice
Cells
Hep G2 Cells
Mitogen-Activated Protein Kinase 1
Cell Survival
Injections

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

引用此文

The hepatic protection effects of hepassocin in hyperglycemic crisis. / Ou, Horng Yih; Wu, Hung Tsung; Lin, Ching Han; Du, Ye Fong; Hu, Che Yuan; Hung, Hao Chang; Wu, Pansee; Li, Hung Yuan; Wang, Shu Huei; Chang, Chih Jen.

於: Journal of Clinical Endocrinology and Metabolism, 卷 102, 編號 7, 01.07.2017, p. 2407-2415.

研究成果: 雜誌貢獻文章

Ou, HY, Wu, HT, Lin, CH, Du, YF, Hu, CY, Hung, HC, Wu, P, Li, HY, Wang, SH & Chang, CJ 2017, 'The hepatic protection effects of hepassocin in hyperglycemic crisis', Journal of Clinical Endocrinology and Metabolism, 卷 102, 編號 7, 頁 2407-2415. https://doi.org/10.1210/jc.2016-3287
Ou, Horng Yih ; Wu, Hung Tsung ; Lin, Ching Han ; Du, Ye Fong ; Hu, Che Yuan ; Hung, Hao Chang ; Wu, Pansee ; Li, Hung Yuan ; Wang, Shu Huei ; Chang, Chih Jen. / The hepatic protection effects of hepassocin in hyperglycemic crisis. 於: Journal of Clinical Endocrinology and Metabolism. 2017 ; 卷 102, 編號 7. 頁 2407-2415.
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abstract = "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.",
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AU - Hu, Che Yuan

AU - Hung, Hao Chang

AU - Wu, Pansee

AU - Li, Hung Yuan

AU - Wang, Shu Huei

AU - Chang, Chih Jen

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N2 - 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.

AB - 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.

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