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
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

Auteurs

Genta Kakiyama (G)

Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA, United States.

Kei Minowa (K)

Department of Pediatrics, Juntendo University Hospital, Tokyo, Japan.

Nanah Bai-Kamara (N)

Internal Medicine, Central Virginia VA Healthcare System, Richmond, VA, United States.

Taishi Hashiguchi (T)

Research and Development Bureau, SMC Laboratories, Tokyo, Japan.

William M Pandak (WM)

Gastroenterology and Hepatology, Central Virginia VA Healthcare System, Richmond, VA, United States.

Daniel Rodriguez-Agudo (D)

Internal Medicine, Virginia Commonwealth University Medical Center, Richmond, VA, United States.

Classifications MeSH