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Steroid-mediated liver steatosis is CD1d-dependent, while steroid-induced liver necrosis, inflammation, and metabolic

Tomer Adar1,2, Ami Ben Ya'acov1,2, Yehudit Shabat1

  • 1Faculty of Medicine, Department of Medicine, Hadassah Medical Center, Hebrew University, POB 1200, 91120, Jerusalem, Israel.

BMC Gastroenterology
|April 8, 2022
PubMed
Abstract

Insights

Glucocorticoids cause non-alcoholic fatty liver disease (NAFLD) and metabolic issues. Glycosphingolipids protect against steroid-induced liver damage, with steatosis being CD1d-dependent but other effects being independent.

Area of Science:

  • Hepatology
  • Immunology
  • Metabolic Diseases

Background:

  • Glucocorticoids are implicated in non-alcoholic fatty liver disease (NAFLD) pathogenesis.
  • Natural killer T cells and CD1d molecules influence NAFLD and steroid response.
  • Glycosphingolipids may offer protection against steroid-induced liver damage.

Purpose of the Study:

  • To investigate the role of CD1d in steroid-induced metabolic dysfunction.
  • To evaluate the protective effects of glycosphingolipids against steroid-induced liver injury.
  • To understand the mechanisms underlying steroid-mediated NAFLD and its complications.

Main Methods:

  • Established a mouse model of oral steroid administration.
  • Assessed the therapeutic effect of β-glucosylceramide (GC) on steroid-induced liver damage and metabolic derangements.
  • Utilized CD1d knockout (CD1d-/-) mice to study the role of CD1d in steroid-induced liver injury and GC's protective effects.

Main Results:

  • Steroid administration induced insulin resistance, hyperinsulinemia, hypertriglyceridemia, liver steatosis, and hepatocellular injury.
  • CD1d-/- mice showed hyperglycemia and hypertriglyceridemia but not significant steatosis after steroid treatment.
  • GC treatment ameliorated steroid-associated metabolic issues and liver injury, irrespective of CD1d expression.

Conclusions:

  • A steroid-induced NAFLD model was developed, highlighting a CD1d-dependent steatosis component.
  • Steroid-induced liver necrosis, inflammation, and metabolic changes were CD1d-independent.
  • Findings suggest a potential dichotomy between steatosis and steatohepatitis in NAFLD pathogenesis.
Keywords:
GlucocerebrosideGlycosphingolipidsNAFLDNASHNKT cellsSteroids

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