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Updated: Oct 13, 2025

A Competent Hepatocyte Model Examining Hepatitis B Virus Entry through Sodium Taurocholate Cotransporting Polypeptide as a Therapeutic Target
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Sodium taurocholate co-transporting polypeptide deficiency.

A L Schneider1, H Köhler2, B Röthlisberger3

  • 1Swiss Pediatric Liver Center, Division of Pediatric Specialties, Department of Pediatrics, Gynecology and Obstetrics, University of Geneva, Geneva, Switzerland.

Clinics and Research in Hepatology and Gastroenterology
|November 10, 2021
PubMed
Summary
This summary is machine-generated.

Na-taurocholate Co-transporting Polypeptide (NTCP) deficiency, caused by SLC10A1 mutations, often presents benignly with elevated bile acids but normal liver enzymes. This review details a novel mutation and discusses the clinical spectrum of this rare inherited bile acid transport disorder.

Keywords:
Failure to thriveHypercholanemiaNTCP deficiency

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Area of Science:

  • Hepatology
  • Genetics
  • Biochemistry

Background:

  • Bile acid transport defects on the basolateral side of hepatocytes are poorly understood.
  • The Sodium-taurocholate Co-transporting Polypeptide (NTCP) encoded by SLC10A1 is a key basolateral bile acid transporter.
  • Previous reports highlight SLC10A1 mutations causing NTCP deficiency with hypercholanemia.

Observation:

  • A female patient presented with failure to thrive and elevated plasma bile acids (up to 150-fold) but normal liver enzymes and bilirubin.
  • Liver biopsies showed unspecific findings, and Autotaxin levels were normal.
  • Genetic analysis revealed a novel homozygous deletion in SLC10A1, predicting complete loss of NTCP function.

Findings:

  • The patient's presentation aligns with previously described cases of NTCP deficiency, emphasizing failure to thrive.
  • Most reported cases with SLC10A1 mutations, particularly the common c.800C>T variant, are asymptomatic, suggesting a generally benign clinical course.
  • Significant variations in plasma bile acid levels exist among patients, potentially due to different mutations or compensatory mechanisms.

Implications:

  • NTCP deficiency is an inherited bile acid transport disorder with a predominantly benign clinical course.
  • Further long-term follow-up is necessary to fully understand the consequences of this condition.
  • Identifying novel mutations expands the known spectrum of NTCP deficiency and aids in understanding bile acid homeostasis.