StarD5 levels of expression correlate with onset and progression of NASH liver fibrosis.
Cholesterol
Fatty liver
Insulin resistance
Transporter
triglycerides
Journal
American journal of physiology. Gastrointestinal and liver physiology
ISSN: 1522-1547
Titre abrégé: Am J Physiol Gastrointest Liver Physiol
Pays: United States
ID NLM: 100901227
Informations de publication
Date de publication:
09 Apr 2024
09 Apr 2024
Historique:
medline:
9
4
2024
pubmed:
9
4
2024
entrez:
9
4
2024
Statut:
aheadofprint
Résumé
Insufficient expression of steroidogenic acute regulatory lipid transfer protein 5 (StarD5) on liver cholesterol/lipid homeostasis is not clearly defined. The ablation of StarD5 was analyzed in mice on a normal or western diet (WD) to determine its importance in hepatic lipid accumulation and fibrosis compared to wild type (WT) mice. Rescue experiments in StarD5 In addition to increased hepatic triglyceride/cholesterol levels, global StarD5 StarD5's downregulation with hepatic lipid excess is a previously unappreciated physiologic function appearing to promote lipid storage for future needs. Conversely, StarD5's lingering downregulation with prolonged lipid/cholesterol excess accelerates fatty liver's transition to fibrosis; mediated via dysregulation in the oxysterol signaling pathway.
Sections du résumé
BACKGROUND AND AIMS
OBJECTIVE
Insufficient expression of steroidogenic acute regulatory lipid transfer protein 5 (StarD5) on liver cholesterol/lipid homeostasis is not clearly defined.
METHODS
METHODS
The ablation of StarD5 was analyzed in mice on a normal or western diet (WD) to determine its importance in hepatic lipid accumulation and fibrosis compared to wild type (WT) mice. Rescue experiments in StarD5
RESULTS
RESULTS
In addition to increased hepatic triglyceride/cholesterol levels, global StarD5
CONCLUSIONS
CONCLUSIONS
StarD5's downregulation with hepatic lipid excess is a previously unappreciated physiologic function appearing to promote lipid storage for future needs. Conversely, StarD5's lingering downregulation with prolonged lipid/cholesterol excess accelerates fatty liver's transition to fibrosis; mediated via dysregulation in the oxysterol signaling pathway.
Identifiants
pubmed: 38591148
doi: 10.1152/ajpgi.00024.2024
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : U.S. Department of Veterans Affairs (VA)
ID : I01 BX005895-01A2
Organisme : VCU | School of Medicine, Virginia Commonwealth University (VCU Med School)
ID : 411456
Organisme : VCU | School of Medicine, Virginia Commonwealth University (VCU Med School)
ID : 411864