|Yuan, Ping -|
|Yu, Ying -|
|Luo, Juan -|
|Tian, Fei -|
|Chang, Shuang -|
|Ramachandran, Ramesh -|
|Song, Jiuzhou -|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 1, 2012
Publication Date: October 1, 2012
Citation: Yuan, P., Yu, Y., Luo, J., Tian, F., Zhang, H., Chang, S., Ramachandran, R., Song, J. 2012. Lipoprotein metabolism differs between Marek's disease susceptible and resistant chickens. Poultry Science. 91:2598-2605. Available: http://ps.fass.org/content/91/10/2598. Interpretive Summary: Marek’s disease (MD) is caused by Marek’s disease virus (MDV). MDV is a widespread oncogenic herpesvirus specifically inducing nerve and/or visceral tumors in susceptible chickens. MD could cause devastated economic loss and remains a serious concern of the poultry industry. MD has been controlled by vaccination. Host genetic resistance to MD has been actively investigated in an effort to augment the current control measure. To advance the understanding of genetic resistance to MD, we examined lipoprotein (a compound contains both proteins and lipids) distributions and the levels of adiponectin (a protein hormone that regulates the metabolism of lipids). Significant differences were detected between MD resistant and susceptible lines of chickens. These findings pave the road for future study to identify new genes or markers conferring MD resistance.
Technical Abstract: Marek’s disease (MD) is a lymphoproliferative disease of chickens caused by MD virus and has an important impact on the poultry industry worldwide.There have been reports showing different physiological characteristics between MD susceptible and resistant chickens. However, little is known about whether there are differences in lipid metabolism between MD susceptible and resistant lines of chickens. In this study, we examined the BW and the weight of tissues (abdomina fat, breast muscle with bone, leg muscle with bone, liver, and heart), the lipoprotein-cholesterol concentrations and distributions, and the plasma and tissue levels of adiponectin and its receptors in the highly resistant showed that the increase in total cholesterol during growth was mainly due to the elevation of cholesterol in the low-density/very low-density lipoprotein fraction in MD susceptible chickens, whereas the increase of total cholesterol was mainly attributable to the increase in high-density lipoprotein-cholesterol in MD resistant chickens. Meanwhile, the MD resistant line appeared to have increased plasma adiponectin levels compared with MD susceptible chickens during growth. Taken together, our data suggested that lipoprotein-cholesterol and adiponectin metabolism are different between MD susceptible and resistant chickens.