The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Defective hepatic regeneration after partial hepatectomy in leptin-deficient mice is not rescued by exogenous leptin.

Liver regeneration after partial hepatectomy (PH) is impaired in leptin-deficient ob/ ob mice. Here, we tested whether exogenous leptin and/or correction of the obese phenotype (by food restriction or long-term leptin administration) would rescue hepatocyte proliferation and whether the hepatic progenitor cell compartment was activated in leptin-deficient ob/ ob livers after PH. Because of the high mortality following 70% PH to ob/ ob mice, we performed a less extensive (55%) resection. Compared to lean mice, liver regeneration after 55% PH was deeply impaired and delayed in ob/ ob mice. Administration of exogenous leptin to ob/ ob mice at doses that restored circulating leptin levels during the surgery and postsurgery period or for 3 weeks prior to the surgical procedure did not rescue defective liver regeneration. Moreover, correction of obesity, metabolic syndrome and hepatic steatosis by prolonged administration of leptin or food restriction (with or without leptin replacement at the time of PH) did not improve liver regeneration in ob/ ob mice. The hepatic progenitor cell compartment was increased in ob/ ob mice. However, after PH, the number of progenitor cells decreased and signs of proliferation were absent from this cell compartment. In this study, we have conclusively shown that neither leptin replacement nor amelioration of the metabolic syndrome, obese phenotype and hepatic steatosis, with or without restitution of normal circulating levels of leptin, was able to restore replicative competence to ob/ ob livers after PH. Thus, leptin does not directly signal to liver cells to promote hepatocyte proliferation, and the obese phenotype is not solely responsible for impaired regeneration.Laboratory Investigation (2006) 86, 1161-1171. doi:10.1038/labinvest.3700474; published online 18 September 2006.[1]

References

  1. Defective hepatic regeneration after partial hepatectomy in leptin-deficient mice is not rescued by exogenous leptin. Leclercq, I.A., Vansteenberghe, M., Lebrun, V.B., Vanhul, N.K., Abarca-Quinones, J., Sempoux, C.L., Picard, C., St??rkel, P., Horsmans, Y.L. Lab. Invest. (2006) [Pubmed]
 
WikiGenes - Universities