CREBH: A Complex Array of Regulatory Mechanisms in Nutritional Signaling, Metabolic Inflammation, and Metabolic Disease

Henry Wade, Kaichao Pan, Qiaozhu Su

Research output: Contribution to journalReview articlepeer-review

1 Scopus citations

Abstract

The endoplasmic reticulum (ER)-resident basic leucine zipper (bZIP) transcription factor c-AMP responsive element binding protein H (CREBH/CREB3L3) is exclusively expressed in the liver and intestine. Physiologically, CREBH is intrinsically linked to nutritional homeostasis via its regulation on fatty acid β-oxidation, lipid droplet process, very low-density lipoprotein metabolism, gluconeogenesis, and iron metabolism. Pathologically, CREBH enhances hepatic acute-phase response gene expression (e.g., C-reactive protein and serum amyloid P-component) and mediates nutrient-surplus induced metabolic inflammation. Hyperactivation of CREBH in metabolic inflammation further contributes to the development of hyperlipidemia, lipotoxicity, non-alcoholic fatty liver disease, and potentially non-alcoholic steatohepatitis. This review highlights recent findings that delineate the interactions between CREBH and peroxisome proliferator activated receptor α (PPARα), fibroblast growth factor 21 (FGF21), fat-specific protein 27 (FSP27), and lipoprotein metabolism with a focus on the molecular and biochemical mechanisms that underlie the development of metabolic inflammation, non-alcoholic fatty liver disease and inflammatory associated bone disease.

Original languageEnglish (US)
Article number2000771
JournalMolecular Nutrition and Food Research
Volume65
Issue number1
DOIs
StatePublished - Jan 2021
Externally publishedYes

Keywords

  • CREBH
  • FGF21
  • FSP27
  • VLDL and metabolic inflammation

ASJC Scopus subject areas

  • Biotechnology
  • Food Science

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