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Compensatory Increase of Serum Hepassocin Protects Hyperthyroidism-Induced Hepatic Dysfunction
Chih-Chen Wang1, Ching-Han Lin1, Hsuan-Wen Chou1
1Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 70101, Taiwan.
This study reveals that serum hepassocin levels decrease with hyperthyroidism treatment. Hepassocin may protect the liver from hyperthyroidism-induced damage by regulating key metabolic enzymes.
Area of Science:
- Endocrinology
- Hepatology
- Molecular Biology
Background:
- Hyperthyroidism frequently causes hepatic dysfunction.
- Hepassocin, a hepatokine, is known for its role in metabolic diseases and liver protection.
- The specific role of hepassocin in hyperthyroidism was previously unclear.
Purpose of the Study:
- To investigate the relationship between hepassocin and hyperthyroidism.
- To explore the protective mechanisms of hepassocin against hyperthyroidism-induced liver injury.
Main Methods:
- Analysis of serum hepassocin and ALT levels in 36 Graves' disease patients before and after treatment.
- In vitro study using HepG2 cells treated with hepassocin recombinant protein and triiodothyronine (T3).
- Assessment of liver enzyme levels (ALT, AST) and PEPCK expression.
Main Results:
- Serum hepassocin concentrations and ALT levels decreased significantly 6 months after hyperthyroidism treatment.
- Hepassocin treatment reduced T3-induced ALT and AST elevation in HepG2 cells.
- Hepassocin dose-dependently increased PEPCK expression, while its deletion reversed T3 effects.
Conclusions:
- A compensatory increase in serum hepassocin may play a protective role in hyperthyroidism-induced hepatic dysfunction.
- T3 upregulates hepassocin expression via a hepatocyte nuclear factor 1α-dependent pathway.
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