Adipogenesis

Abstract

Adipose tissue is an important site for lipid storage, energy homeostasis, and whole-body insulin sensitivity. It is important to understand the mechanisms involved in adipose tissue development and function, which can be regulated by the endocrine actions of various peptide and steroid hormones. Recent studies have revealed that white and brown adipocytes can be derived from distinct precursor cells. This review will focus on transcriptional control of adipogenesis and its regulation by several endocrine hormones. The general functions and cellular origins of adipose tissue and how the modulation of adipocyte development pertains to metabolic disease states will also be considered.

Figure 1.

Transcription factors that are positive and negative effectors of adipocyte development. Many transcription factors are induced during adipocyte differentiation. Some of these, like members of the AP-1 family, are induced during clonal expansion. Other transcription factors, like PPARγ, promote adipocyte differentiation. Adipocyte development is also influenced by several transcription factor families that have negative effects on adipogenesis.

Figure 2.

White and brown adipocytes are derived from distinct precursor cells and have distinct morphological characteristics. White adipocytes can be derived from mesenchymal precursor cells. Brown adipocytes are derived from Myf5-expressing precursor cells. Mature brown adipocytes contain multilocular lipid droplets and are mitochondria rich. PRDM16 is present in both brown and white adipocytes and is an important factor in transforming white adipocytes to beige adipocytes.

Figure 3.

Proinflammatory cytokines produced from immune cells in unhealthy adipose tissue inhibit adipocyte development. The adipocytes in healthy adipose tissue are insulin sensitive, and the tissue does not contain TNFα- and IFNγ-producing cells. The adipocytes in metabolically unhealthy adipose tissue are insulin resistant and lack the normal ability to expand. The presence of infiltrated immune cells that produce TNFα and IFNγ results in inhibition of adipocyte development.