What is it about?
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. In the current study, we investigated whether the increased liver hormone (hepassocin) secretion in hyperglycemic crisis might offset the deleterious effects of hyperglycemia on hepatocytes.
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Why is it important?
This is the first study to explore the hepatic protection effect of liver-derived hepatokine, hepassocin, in hyperglycemia. We found that hyperglycemia induced hepassocin expression to exert a protective effect on the liver by increasing anti-oxidative stress, based on the results of human, cell, and animal studies.
Perspectives
In this work, we provide evidence to clarify the pathophysiological role of hepassocin in hyperglycemic crisis. Hepassocin increases anti-oxidative stress proteins to protect hepatocytes from high glucose-induced glucotoxicity. Moreover, the increased hepassocin levels might be involved in the development of extreme insulin resistance in hyperglycemic crisis.
Horng-Yih Ou
National Cheng Kung University
Read the Original
This page is a summary of: The Hepatic Protection Effects of Hepassocin in Hyperglycemic Crisis, The Journal of Clinical Endocrinology & Metabolism, April 2017, Endocrine Society,
DOI: 10.1210/jc.2016-3287.
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