Adipogenesis

Transcription factors, peroxis proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding proteins (C/EBPs) are main regulators of adipogenesis.

The key features of differentiated adipocytes are growth arrest, morphological change, high expression of lipogenic genes and production of adipokines like adiponectin, leptin, resistin (in the mouse, not in humans) and TNF-alpha.

The growth arrest followed by the earliest events, including a morphological change of preadipocyte from the fibroblast-shape to the round-shape and the induction of transcription factors C/EBPβ, and C/EBPδ.

These genes include adipocyte protein (aP2), insulin receptor, glycerophosphate dehydrogenase, fatty acid synthase, acetyl CoA carboxylase, glucose transporter type 4 (Glut 4) and so on.

PPARγ heterodimerizes with retinoid X receptor (RXR) and then binds to DNA, which activates the promoters of the downstream genes.

PPARg activation has effects on several aspects of the mature adipocyte characteristics such as morphological changes, lipid accumulation, and the acquisition of insulin sensitivity.

[25] At the early stage of differentiation, the transient increase of C/EBPβ and C/EBPδ mRNA and protein levels are thought to activate the adipogenic transcription factors, PPARγ and C/EBPα.

T-cell factor/lymphoid enhancer-binding factor (TCF/LEF),[28] GATA2/3,[29] retinoic acid receptor α,[30] and SMAD6/7[31] don't affect the expression of C/EBPβ and C/EBPδ but inhibit the induction of PPARγ and C/EBPα.

Products of endocrine system such as insulin, IGF-1, cAMP, glucocorticoid, and triiodothyronine effectively induce adipogenesis in preadipocytes.

Wnt/β-catenin signaling suppresses adipogenesis, by promoting the differentiation of mesenchymal stem cells into myocytes and osteocytes but blocking the commitment to the adipocytic lineage.

Bone morphogenetic proteins (BMPs) are transforming growth factor β (TGFβ) superfamily members.