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and Cd36 deficient mice have lower body mass (Kevorkova et al., 2013) and decreased adipogenesis (Vroegrijk et al., 2013). Our results indicate decreased plasma leptin levels without any changes in adiponectin levels in Cd36-nuli mice. Moreover, the body mass-to-leptinemia correlation, usually positive (Monti et al., 2006), is severely stunted in the three month-old nuli mice. There are discrepancies conceming leptin levels in the Cd36-nuli mouse model, which has been reported to be either hypo- (Ibrahimi, 2003) or hyperleptinemic (Hajri et al., 2007). These differences could be linked to diet type and various level of physical activity; however, genetic context has likely the most impact, as each strain shows different basal metabolism levels (Śedov£ et al., 2012). Either condition however points towards disrupted energetic balance mainly linked to the fatty acid uptake functions of CD36 (Hajri et al, 2007).

As it was previously shown, Cd36-nuli MSCs have reduced osteogenic potential (Kevorkova et al., 2013). Since leptin is known to couple energy and bonę homeostasis (Karsenty, 2006; Yadav et Karsenty, 2009), namely during the endochondral ossification process (Kurne et al., 2002; Kishida et al., 2005), we investigated whether leptin and chondrogenic markers expression in marrow cells was altered by CD36 deficiency. Our results indicate decreased leptin expression yet an increase of chondrogenic transcription factor Sox9 in MSCs derived from Cd36-null mice. However, the expression of Col-IIa, a marker of maturę chondrocyte, and growth piąte morphology did not indicate any other alteration. Interestingly, previous data showed decreased Osx and Runx2 gene expression by Cd36-nuli MSCs (Kevorkova et al, 2013). The expression of both markers in osteoblasts is influenced by exposure to leptin (Zhou et al, 2012) or by circulating leptin levels (Kalra et al, 2009). Combined with the present data, these alterations can indicate a delayed transition from osteochondroprogenitor to osteoblast manifested by increased chondrocyte recruitment and an increase in cartilage growth piąte. Growth piąte thickness was comparable for Cd36-nuli and WT mice. The hypertrophic zonę was