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Glycochenodeoxycholate Affects Iron Homeostasis via Up-Regulating Hepcidin Expression.

Long-Jiao Wang1, Guo-Ping Zhao2, Xi-Fan Wang1

  • 1Key Laboratory of Functional Dairy, Co-Constructed by Ministry of Education and Beijing Municipality, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China.

Nutrients
|August 12, 2022
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Summary
This summary is machine-generated.

Abnormal levels of Glycochenodeoxycholate (GCDCA) increase hepcidin expression, impacting iron homeostasis in chronic kidney disease (CKD) patients. GCDCA activates the FXR-SMAD signaling pathway, potentially causing iron deficiency in CKD.

Keywords:
SMAD1/5/8farnesoid X receptorglycochenodeoxycholatehepcidiniron homeostasis

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Area of Science:

  • Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Hepcidin regulates iron homeostasis, and its increased expression is linked to iron deficiency in chronic kidney disease (CKD).
  • Abnormal serum steroid levels are implicated in elevated hepcidin, but the specific role of Glycochenodeoxycholate (GCDCA) remains unclear.

Purpose of the Study:

  • To investigate the correlation between Glycochenodeoxycholate (GCDCA) and hepcidin expression in patients with chronic kidney disease (CKD).
  • To elucidate the underlying molecular mechanisms by which GCDCA influences hepcidin levels and iron homeostasis.

Main Methods:

  • Measured serum hepcidin, iron, and GCDCA levels in CKD patients and healthy controls.
  • Utilized HepG2 cells to assess GCDCA's effect on hepcidin expression and signaling pathways (SMAD, STAT3, CREBH, FXR).
  • Administered varying doses of GCDCA to C57/BL6 mice to evaluate in vivo effects on hepcidin, hemoglobin, and serum iron.

Main Results:

  • CKD patients exhibited higher GCDCA and hepcidin levels, with decreased serum iron.
  • In vitro, GCDCA treatment significantly increased hepcidin expression in HepG2 cells by activating the FXR-BMP6/ALK3-SMAD signaling pathway.
  • In vivo, GCDCA administration in mice elevated hepcidin and reduced hemoglobin and serum iron levels, confirming the FXR-SMAD pathway's role.

Conclusions:

  • Glycochenodeoxycholate (GCDCA) is a potential inducer of hepcidin expression, contributing to iron homeostasis imbalance in CKD.
  • The mechanism involves GCDCA activating the farnesoid X receptor (FXR) and subsequently the BMP6/ALK3-SMAD signaling pathway.
  • Elevated GCDCA levels may serve as a biomarker for iron deficiency risk in CKD patients.