Distinction of white, beige and brown adipocytes derived from mesenchymal stem cells - PubMed (original) (raw)

Review

Distinction of white, beige and brown adipocytes derived from mesenchymal stem cells

Anna Park et al. World J Stem Cells. 2014.

Abstract

Adipose tissue is a major metabolic organ, and it has been traditionally classified as either white adipose tissue (WAT) or brown adipose tissue (BAT). WAT and BAT are characterized by different anatomical locations, morphological structures, functions, and regulations. WAT and BAT are both involved in energy balance. WAT is mainly involved in the storage and mobilization of energy in the form of triglycerides, whereas BAT specializes in dissipating energy as heat during cold- or diet-induced thermogenesis. Recently, brown-like adipocytes were discovered in WAT. These brown-like adipocytes that appear in WAT are called beige or brite adipocytes. Interestingly, these beige/brite cells resemble white fat cells in the basal state, but they respond to thermogenic stimuli with increased levels of thermogenic genes and increased respiration rates. In addition, beige/brite cells have a gene expression pattern distinct from that of either white or brown fat cells. The current epidemic of obesity has increased the interest in studying adipocyte formation (adipogenesis), especially in beige/brite cells. This review summarizes the developmental process of adipose tissues that originate from the mesenchymal stem cells and the features of these three different types of adipocytes.

Keywords: Adipogenesis; Beige/brite adipocytes; Brown adipocytes; Browning; Mesenchymal stem cells; Thermogenesis; White adipocytes.

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Figures

Figure 1

Figure 1

Locations of adipose tissue depots in a mouse (A) and an adult human (B). A: Subcutaneous (inguinal and intramuscular), visceral (mesenteric, omental, perigonadal and retroperitoneal) and brown (interscapular and perirenal) adipose tissue depots are shown in a mouse model; B: Subcutaneous (abdominal, femoral and gluteal), visceral (epicardial, gonadal, mesenteric, omental and retroperitoneal) and brown (paravertebral, supraclavicular and suprarenal) adipose tissue depots are shown in a human model. WAT: White adipose tissue; BAT: Brown adipose tissue.

Figure 2

Figure 2

Differentiation into white, beige or brown adipocytes. Previously, white and brown adipocytes were thought to be derived from the same precursor cell. However, recent studies demonstrated that brown fat shares a progenitor cell (Myf5+) with skeletal muscle and not with white adipocytes. The Myf5+ precursors are induced to transform into mature brown adipocytes by bone morphogenetic protein 7 (BMP7), peroxisome proliferator-activated receptor-γ (PPAR-γ) and CCAAT/enhancer-binding proteins (C/EBPs) in cooperation with the transcriptional co-regulator PR domain-containing 16 (PRDM16) and PGC-1α. White adipocytes can also be transformed to brown-like adipocytes, called beige/brite adipocytes, by cold exposure, a β-adrenergic agonist or a PPAR-γ agonist. AR: adrenergic receptor; FGF21: Fibroblast growth factor 21; PGC-1α: Peroxisome proliferator activated receptor gamma coactivator 1 alpha.

Figure 3

Figure 3

Key regulators of the browning process and their action mechanisms. Browning is induced by sympathetic nervous system (SNS)-independent or SNS-dependent signals. These signals sometimes synergistically or competitively influence the activation of browning of subcutaneous white adipose tissue (sWAT). Irisin is a newly discovered myokine and is released by skeletal muscle during exercise. Irisin induces the browning process of sWAT. Fibroblast growth factor-21 (FGF21), a hormonal factor from the liver, directly activates the thermogenic process via interaction with the FGF receptor/β-Klotho (KLB) complex. The norepinephrine secreted by the SNS in response to thermogenic stimuli induces the activation of adrenergic receptor(s). The adrenergic receptor-mediated signal increases the level of intracellular cAMP and activates cAMP-dependent protein kinase A (PKA). Subsequently, PKA activates p38 MAP kinase (p38 MAPK) and 5’-deiodinase 2 (Dio2), which catalyzes the conversion of thyroxine (T4) into the active form 3,5,3’-tri-iodothyronine (T3). Then, it ultimately induces the gene process for thermogenic activation. Natriuretic peptides (NPs) originating from the heart activate the thermogenic process through binding to the NP receptor, activation of protein kinase G (PKG) and the subsequent activation of p38 MAPK and NPR. NPR: Natriuretic peptides receptor; TAG: Triacylglycerol; FA: Fatty acid.

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