Key result
The molecular control of adipogenesis involves a complex transcriptional cascade regulated by PPARgamma and C/EBP family members, with implications for lymphatic pathology.
This review summarizes the transcriptional cascade regulating adipogenesis, including PPARgamma and C/EBP family members, and discusses the relationship between adipose depots and the lymphatic system.
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Should not yet change lymphatic disease management; leaves open targeted investigation of PPARgamma/C/EBP pathways in adipose-lymphatic interactions.
Adipogenesis is the process by which mature fat cells are formed from pre-adipocytes. Adipogenesis has come under increasing scrutiny not only because the availability of reliable in vitro models makes it an attractive choice for developmental studies, but also because adipocytes are increasingly recognized as major players in a variety of physiological and pathophysiological states, such as obesity and type 2 diabetes. Adipocytes develop from mesenchymal stem cell precursors that are characterized by multipotency. Under the influence of various cues, these cells become committed to the adipocyte lineage. Further hormonal stimulation recruits these pre-adipocytes to accumulate lipid, express fat-specific markers, and become sensitive to the metabolic effects of insulin. A complex transcriptional cascade regulates this process, involving several distinct classes of transcription factor. In particular, the role of the nuclear hormone receptor PPARgamma will be discussed, along with bZip family members C/EBPalpha, C/EBPbeta, and C/EBPdelta. The relationship of adipose depots to the lymphatic system will also be discussed.
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Evan D. Rosen (2002) conducted a review in Adipogenesis and lymphatic pathology. The molecular control of adipogenesis involves a complex transcriptional cascade regulated by PPARgamma and C/EBP family members, with implications for lymphatic pathology.
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