The hepatic protection effects of hepassocin in hyperglycemic crisis.

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The hepatic protection effects of hepassocin in hyperglycemic crisis.

J Clin Endocrinol Metab. 2017 Apr 11;:

Authors: Ou HY, Wu HT, Lin CH, Du YF, Hu CY, Hung HC, Wu P, Li HY, Wang SH, Chang CJ

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, SETTINGS, AND PATIENTS: Plasma hepassocin concentrations and routine biochemistry were measured in twenty-one 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 anti-oxidative stress proteins, including superoxide dismutase 1 (SOD1). In HepG2 cells, high glucose increased hepassocin expression through STAT3 and hepatocyte nuclear factor (HNF)-related pathways. We also demonstrated that hepassocin increased SOD1 expression through an ERK1/2-NRF2 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.

PMID: 28402540 [PubMed - as supplied by publisher]

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