Transcriptional Regulation of Adipogenesis

Abstract

Adipocytes are the defining cell type of adipose tissue. Once considered a passive participant in energy storage, adipose tissue is now recognized as a dynamic organ that contributes to several important physiological processes, such as lipid metabolism, systemic energy homeostasis, and whole-body insulin sensitivity. Therefore, understanding the mechanisms involved in its development and function is of great importance. Adipocyte differentiation is a highly orchestrated process which can vary between different fat depots as well as between the sexes. While hormones, miRNAs, cytoskeletal proteins, and many other effectors can modulate adipocyte development, the best understood regulators of adipogenesis are the transcription factors that inhibit or promote this process. Ectopic expression and knockdown approaches in cultured cells have been widely used to understand the contribution of transcription factors to adipocyte development, providing a basis for more sophisticated in vivo strategies to examine adipogenesis. To date, over two dozen transcription factors have been shown to play important roles in adipocyte development. These transcription factors belong to several families with many different DNA-binding domains. While peroxisome proliferator-activated receptor gamma (PPARγ) is undoubtedly the most important transcriptional modulator of adipocyte development in all types of adipose tissue, members of the CCAAT/enhancer-binding protein, Krüppel-like transcription factor, signal transducer and activator of transcription, GATA, early B cell factor, and interferon-regulatory factor families also regulate adipogenesis. The importance of PPARγ activity is underscored by several covalent modifications that modulate its activity and its ability to modulate adipocyte development. This review will primarily focus on the transcriptional control of adipogenesis in white fat cells and on the mechanisms involved in this fine-tuned developmental process. © 2017 American Physiological Society. Compr Physiol 7:635-674, 2017.

Fructose, Glucocorticoids and Adipose Tissue: Implications for the Metabolic Syndrome

“…In the last couple of decades, the cellular and molecular mechanisms of adipocyte differentiation have been extensively studied and various hormones and growth factors affecting adipocyte differentiation in a positive or negative manner have been identified [9,73,74,75,76,77,78]. Although several clinical and in vitro studies defined the high lipogenicity of fructose and its stimulation of adipogenesis [19,79,80], further questions were raised on the exact mechanisms and regulatory factors involved behind this phenomenon.…”

Flavonoids from Acer okamotoanum Inhibit Adipocyte Differentiation and Promote Lipolysis in the 3T3-L1 Cells

“…C/EBPs and PPARs family are essential factors for adipogenesis [6]. Adipogenesis accelerates differentiation of preadipocytes into adipocytes, resulting in intracellular lipid accumulation [5,6].…”

“…Adipogenesis is the process to become adipocytes mature from preadipocytes, and it is regulated by adipogenic key transcription factors including family of CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptors (PPARs) [6]. During adipogenesis process, adipogenic key transcription factors enhance the lipogenic enzymes such as fatty acid synthase (FAS) and adipocytes protein 2 (aP2) [7,8].…”

p ‐Synephrine exhibits anti‐adipogenic activity by activating the Akt/GSK3β signaling pathway in 3T3‐L1 adipocytes

“…PPARγ controls the adipogenic process and upregulates the downstream gene aP2, which is the adipogenesis-and lipid metabolism-associated gene (Mota de Sa, Richard, Hang, & Stephens, 2017).…”