| First Author | Ghosh S | Year | 2010 |
| Journal | Hepat Med | Volume | 2010 |
| Issue | 2 | Pages | 69-78 |
| PubMed ID | 21949477 | Mgi Jnum | J:285507 |
| Mgi Id | MGI:6400487 | Doi | 10.2147/HMER.S8902 |
| Citation | Ghosh S, et al. (2010) Mice with null mutation of Ceacam I develop nonalcoholic steatohepatitis. Hepat Med 2010(2):69-78 |
| abstractText | Transgenic liver-specific inactivation of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM1) impairs hepatic insulin clearance and causes hyperinsuline-mia, insulin resistance, elevation in hepatic and serum triglyceride levels, and visceral obesity. It also predisposes to nonalchoholic steatohepatitis (NASH) in response to a high-fat diet. To discern whether this phenotype reflects a physiological function of CEACAM1 rather than the effect of the dominant-negative transgene, we investigated whether Ceacam1 (gene encoding CEACAM1 protein) null mice with impaired insulin clearance also develop a NASH-like phenotype on a prolonged high-fat diet. Three-month-old male null and wild-type mice were fed a high-fat diet for 3 months and their NASH phenotype was examined. While high-fat feeding elevated hepatic triglyceride content in both strains of mice, it exacerbated macrosteatosis and caused NASH-characteristic fibrogenic changes and inflammatory responses more intensely in the null mouse. This demonstrates that CEACAM1-dependent insulin clearance pathways are linked with NASH pathogenesis. |
