By Susanne Klaus
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Additional resources for Adipose Tissues
Adipoblasts are fibroblast-like cells and no specific markers of that stage have been identified so far. Growth arrest leads to the emergence of early markers of differentiation and to the formation of preadipose cells that have not yet accumulated neutral lipids. Terminal differentiation of preadipocytes into adipocytes leads to the emergence of a very large set of markers which are enzymes and proteins involved in lipid accumulation and mobilization, resulting in the formation of triacylglycerol-containing cells.
Terminal differentiation (defined by the emergence of GPDH activity and triacylglycerol accumulation) then takes place, providing that cells are exposed to the appropriate hormonal milieu. 2 During adipocyte differentiation, the dramatic changes observed in cell morphology are associated with alterations in extracellular matrix components. 5 So far, three families of transcriptional activators are known to be induced during adipogenesis. Among members of the first family, PPAR∃ (= PPAR∀ = NUC-1 = FAAR) emerges rapidly at confluence followed during clonal expansion by the emergence of PPAR#.
In addition to IGF-1, clonal and primary preadipocytes also secrete insulin-like growth factor binding proteins (IGFBPs) as a function of differentiation. The IGF-1/IGFBPs system is assumed to act in a paracrine/autocrine manner upon GH stimulation, although conflicting results have been reported with respect to the adipogenic activity of GH in vitro. 104,105 However GH appears to have an additional effect besides stimulating mitoses through IGF-1 production. Growth hormone promotes diacylglycerol production from phosphatidylcholine breakdown and thus activates protein kinase C activity (PKC).
Adipose Tissues by Susanne Klaus