|Wu, Ying-Jen - TEXAS A&M UNIVERSITY|
|Wright, J - GEORGIA SW STATE UNIV|
|Cartwright, A - TEXAS A&M UNIVERSITY|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 28, 2000
Publication Date: January 28, 2000
Interpretive Summary: Chickens are a popular and efficient source of lean meat. Selection for increased body weight or increased growth rate in chickens improves production efficiency, but often yields excessive fat deposition. Excessive fat deposition negatively affects feed cost, animal health, consumer acceptance, and sale of poultry products. Consequently, a reduction of fat in poultry is considered desirable. One way to reduce such body fat is by the use of specialized blood proteins, termed antibodies. In this study, antibodies were raised against chicken fat cell membranes. These antibodies were used, in tissue culture, to reduce fat cell cluster number, cell size, or cluster size of chicken fat cells. These results are potentially valuable for the poultry industry, since by using these antibodies it may be possible to reduce the body fat content of broiler chickens. Ultimately, this could lead to a healthier food product for the consumer.
Technical Abstract: Monoclonal antibodies (Mabs) raised against embryonic chicken adipocyte plasma membranes were used to investigate complement-mediated cytotoxicity or inhibition of differentiation of adipocytes and preadipocytes in primary stromal-vascular (SV) cultures. Adipocyte precursor cells were obtained for primary culture from 18-day chick embryos by collagenase digestion. Cultures were maintained in Medium 199 supplemented with 5% fetal bovine serum for 4 days. Subsequently, the medium was replaced with Medium 199 supplemented with 10% chicken serum to initiate adipocyte differentiation. At day 5 post inoculation, individual or combinations of Mabs were administered to preadipocyte culture wells; rabbit complement was added 30 min later. After one day of incubation, four of the six Mabs with complement significantly (P<0.05) reduced the number of fat cell clusters that developed in culture by 40-60%. These Mabs, in the presence of complement, also significantly (P<0.05) reduced mean cell width, and apparent cell area or cell cluster area of lipid-containing cells. Neither Mab nor complement alone-reduced fat cell cluster number, cell size, nor cluster size. Treatment with pools of either 2 or 4 of the Mabs decreased the total amount of Mab protein concentration required to effectively reduce fat cell cluster number. Four antibodies, used separately, or in combination, reduced fat cell cluster development in a complement- dependent manner.