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Title: Progeny from dedifferentiated adipocytes display protracted adipogenesis

Author
item FERNYHOUGH, MELINDA - Washington State University
item Hausman, Gary
item DODSON, MICHAEL - Washington State University

Submitted to: Journal of Cells Tissues and Organs
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/20/2008
Publication Date: 10/1/2008
Citation: Fernyhough, M.E., Hausman, G.J., Dodson, M.V. 8008. Progeny from dedifferentiated adipocytes display protracted adipogenesis. Journal of Cells Tissues and Organs. 188(4):359-72.

Interpretive Summary: Studies of fat cells converting to non-fat cells and then becoming fat cells again are limited by a poor understanding of the biology of this process. Key biological aspects of this process are detailed and illustrated. The availability of this information will allow critical examination of the process of fat cells becoming fat cells after converting to non-fat cells. Understanding regulation of this process will ultimately lead to means to control fat deposition in the meat animal.

Technical Abstract: Progeny of adipofibroblast cells, derived from mature bovine adipocytes, were used to determine their ability to redifferentiate into lipid-assimilating adipocytes. Traditional cell biology methods were used, including the expression of adipogenic markers such as PPAR'. When exposed to medium supplemented with fetal bovine serum, but not horse serum, cells began to form structures reminiscent of foci. Horse serum supplemented medium resulted in a slowed progression towards cell conversion to lipid-assimilating adipocytes. When analyzed, the horse serum was found to contain more cortisol, IGF-I, as well as differing fatty acid ratios. Histological observations of the horse serum treated cultures (alone), cultures treated with a traditional differentiation induction medium (dexamethasone, methylisobutylxanthine and insulin), treated with insulin +/- different lipid compounds, or treated with a PPAR' agonist (rosiglitazone) resulted in the presence of intracellular vesicles, of which some contained lipid and some did not. Vesicles that did not stain for lipid did not possess glycogen or other types of storage moieties; even though the cells expressed cellular markers deeming them to be differentiated adipocytes (PPAR' protein and mRNA were expressed by cells possessing vesicles, as were hormone sensitive lipase and lipoprotein lipase). Non-lipid filled intracellular vesicle walls possessed the structural protein perilipin. These results are supportive of the progeny adipofibroblasts representing a unique adipogenic model that displays protracted adipogenesis.