| First Author | Zhang J | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 450 |
| Issue | 4 | Pages | 1619-25 |
| PubMed ID | 25035929 | Mgi Jnum | J:317642 |
| Mgi Id | MGI:6855651 | Doi | 10.1016/j.bbrc.2014.07.048 |
| Citation | Zhang J, et al. (2014) PKCdelta regulates hepatic triglyceride accumulation and insulin signaling in Lepr(db/db) mice. Biochem Biophys Res Commun 450(4):1619-25 |
| abstractText | PKCdelta has been linked to key pathophysiological features of non-alcoholic fatty liver disease (NAFLD). Yet, our knowledge of PKCdelta's role in NAFLD development and progression in obese models is limited. PKCdelta(-/-)/Lepr(db)(/)(db) mice were generated to evaluate key pathophysiological features of NAFLD in mice. Hepatic histology, oxidative stress, apoptosis, gene expression, insulin signaling, and serum parameters were analyzed in Lepr(db)(/)(db) and PKCdelta(-/-)/Lepr(db)(/)(db) mice. The absence of PKCdelta did not abrogate the development of obesity in Lepr(db)(/)(db) mice. In contrast, serum triglyceride levels and epididymal white adipose tissue weight normalized to body weight were reduced in PKCdelta(-/-)/Lepr(db)(/)(db) mice compared Lepr(db)(/)(db) mice. Analysis of insulin signaling in mice revealed that hepatic Akt and GSK3beta phosphorylation were strongly stimulated by insulin in PKCdelta(-/-)/Lepr(db)(/)(db) compared Lepr(db)(/)(db) mice. PKCdelta may be involved in the development of obesity-associated NAFLD by regulating hepatic lipid metabolism and insulin signaling. |
