By Susanne Klaus
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D. D. D. D. D. D. + (+) 37,38 RAR! and RAR# + ++ +++ 68 RXR! and RXR∀ + ++ +++ 68 TR + + ++ 114,115 PPAR∃ - + ++ 67 PPAR# - (+) ++ 54 AhR + (+) - 158-161 Arnt + (+) - 158,159 continued on next page The ability of retinoic acid (RA) and synthetic retinoids to promote or inhibit differentiation processes has been recognized for several years. At supraphysiological concentrations, RA inhibits adipogenesis of clonal and primary preadipocytes via RA receptors (RARs). 67 Fatty acids have been shown to act as hormones as the main adipogenic component of serum that has been identified is arachidonic acid (AA).
16 Some controversy exists, however, as to whether the formation of new fat cells takes place during refeeding after a prolonged period of food deprivation. 20 This conclusion goes against the current tide of apoptosis of white adipocytes. In vitro it is clear that human preadipocytes and adipocytes undergo apoptosis in response to serum deprivation or tumor necrosis factor-! 21,22 Tumor necrosis fator-! 2. Multiple stages of adipose cell differentiation. The scheme is based upon data obtained with 3T3-L1, 3T3-F442A, and Ob17 cells as well as with rodent adipose precursor cells.
During the postnatal period, numerous studies using 3H-thymidine have been performed in order to distinguish between cell proliferation and the lipid-filling process. 10 Moreover the highest labeling index is observed in cells negative for GPDH, a late marker of adipose cell differentiation. 11 Thus it appears that early marker-expressing cells undergo mitoses before terminal differentiation and lipid filling take place. However a late hyperplastic development of WAT still remains possible. 12 The life-long potential to make new fat cells has been clearly illustrated in rodents.