Bibliographic Details
| Title: |
Hepatic IR and IGF1R signaling govern distinct metabolic and carcinogenic processes upon PTEN deficiency in the liver |
| Authors: |
Monika Gjorgjieva, Nicolas Calo, Cyril Sobolewski, Dorothea Portius, Jean-Luc Pitetti, Flavien Berthou, Anne-Sophie Ay, Marion Peyrou, Lucie Bourgoin, Christine Maeder, Margot Fournier, Marta Correia de Sousa, Etienne Delangre, Laurent Vinet, Xavier Montet, Christine Sempoux, Serge Nef, Michelangelo Foti |
| Source: |
JHEP Reports, Vol 7, Iss 4, Pp 101305- (2025) |
| Publisher Information: |
Elsevier, 2025. |
| Publication Year: |
2025 |
| Collection: |
LCC:Diseases of the digestive system. Gastroenterology |
| Subject Terms: |
Hepatic metabolism, Hepatocarcinogenesis, Insulin receptor, IGF-1 receptor, Steatosis, Diseases of the digestive system. Gastroenterology, RC799-869 |
| More Details: |
Background & Aims: Hepatocyte-specific deficiency of the phosphatase and tensin homolog (PTEN) triggers steatosis and the development of hepatic tumors. The hepatoprotective effect of PTEN may partly depend on its ability to block insulin receptor (IR) and insulin-like growth factor 1 receptor (IGF1R) signaling. This study aimed to evaluate the individual/combined contributions of IR and IGF1R to hepatic metabolism and tumorigenesis induced by PTEN deficiency. Methods: Mouse models with hepatocyte-specific deletions of Insr, Igf1r, or both, in addition to Pten, were used to investigate the distinct/combined roles of IR and IGF1R. Analyses focused on the impact of these deletions on hepatic steatosis and metabolism, whole-body adiposity, and liver tumor incidence. Results: IR and IGF1R signaling contribute to steatosis induced by Pten ablation through distinct mechanisms. Hepatic IGF1R regulates hepatic glucose output and glycogen storage (2.1-fold increase in hepatic glycogen in PTEN-IGF1RKO mice [n = 10], compared with PTENKO mice [n = 7], p |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2589-5559 |
| Relation: |
http://www.sciencedirect.com/science/article/pii/S2589555924003094; https://doaj.org/toc/2589-5559 |
| DOI: |
10.1016/j.jhepr.2024.101305 |
| Access URL: |
https://doaj.org/article/47a94198f8ab42a1b3859fc35f55af3e |
| Accession Number: |
edsdoj.47a94198f8ab42a1b3859fc35f55af3e |
| Database: |
Directory of Open Access Journals |
