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translocates to the nucleus, associates with the TCF/Lef and regulates the expression of Wnt target-genes (Travis et al., 1991). Via this mechanism, Wnt/p-catenin signaling promotes the progression of cells to bone-producing osteoblasts. Also, RSPO act as secreted Wnt agonists that potentiate Wnt signaling through binding to leucine-rich repeat-containing G protein-coupled receptor which then acts as co-receptors with FZD and LRP5/6 (Kazanskaya et al., 2004). On the other hand, the Wnt pathway is also submitted to negative regulation as it is antagonized by extracellular factors such as SOST (encoded by the Sost gene) and DKK1 (Kawano et Kypta, 2003; Li et al., 2005).

We have recently reported that cluster of differentiation 36 deficient (Cd36-nuli) mice show Iow bonę mass in femur and vertebrae from 2 to 6 month-old mice (Kevorkova et al., 2013). CD36 is a cell-surface membranę glycoprotein of the class B scavenger receptor family expressed by a variety of tissues and cells, and binds various extracellular ligands such as oxidized low-density lipoprotein, thrombospondin-1 (TSP-1), growth hormone releasing peptides, hexarelin, fibrillar Ap amyloid peptides and long-chain fatty acids (LCFA) (Park 2014). CD36 is involved in energy metabolism, atherosclerosis, angiogenesis, immunity and behaviour (Febbraio et al., 2001; Silverstein et Febbraio 2009). The inhibition of angiogenesis is one of the most well-established functions of CD36. Following binding of TSP-1, CD36 expressed by microvascular endothelial cells initiates anti-angiogenic signals that lead to inhibition of adhesion, migration and proliferation of endothelial cells, and induction of their apoptosis (Dawson et al., 1997). As a LCFA translocase, CD36 regulates the fatty acid uptake in adipose tissue, and growth and proliferation of adipocytes (Cobum et al., 2000; Vroegrijk et al., 2013). Adipose cells are recognized to secrete the hormone leptin (Park et Ahima, 2014) that exerts a dual effect on bonę homeostasis. Through central hypothalamic adrenergic p2 signaling, leptin negatively regulates bonę by increasing the production of RANKL that activates the proliferation of osteoclasts and bonę resorption (Takeda et al., 2002). Peripheral leptin increases bonę mass via

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