“…Prostaglandin F2a [Russell and Ho, 1976], prostacyclin [Négrel et al, 1989], 1-methyl-3-isobutyl xanthine (MIX) [Russell and Ho, 1976], dexamethasone (DEX) [Rubin et al, 1978] or indomethacin [Williams and Polakis, 1977] accelerate the expression of the adipose phenotype. Insulin, IGF-1 and L-T3 increase clonal expansion and regulate the lipogenic enzyme activities of terminally differentiated adipocytes [Steinberg and Brownstein, 1982;Zezulak and Green, 1985;Flores-Delgado et al, 1987;Guller et al, 1988;Dani et al, 1989], whereas growth hormone (GH) [Morikawa et al, 1982[Morikawa et al, , 1984Nixon and Green, 1984] and serum adipogenic factors [Kuri-Harcuch and Green, 1978;Hauner and Lö ffler, 1986;Kuri-Harcuch, unpublished results], seem to be involved in promoting commitment [Castro-Muñ ozledo et al, 2003]. Interferon-g [Keay and Grossberg, 1980], retinoids [Murray and Russell, 1980;Kuri-Harcuch, 1982;Castro-Muñ ozledo et al, 1987], TGF-b [Ignotz and Massague, 1985], and TNFa [CastroMuñ ozledo et al, 2003] inhibit adipocyte differentiation.…”