3513659778

3513659778



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However, following dissection we noticed that visceral and fat pad adipose tissues were globally reduced in Cd36KO mice compared to WT (unpublished observations) which may account for the reduced weight of Cd36KO mice. In accordance with our observation, lower weight and decreased total body fat in małe Cd36KO mice have been previously reported (Hajri et al.y 2007). To notę, CD36 deficiency has been associated to impaired differentiation of adipocytes, adipocyte hypotrophy and reduction in their numbers in adipose tissue (Christiaens et al.y 2012). In another study, Iow weight of Cd36KO mice was related to impaired CD36-mediated uptake of fatty acids to the peripheral, and particularly, to the adipose tissue (Goudriaan et al.y 2003). Thus, decreased body weight in Cd36KO animals may be a conseąuence of disturbance in the delivery of fatty acids and/or impaired adipogenesis. Low body weight is an established risk factor for low bonę mass and fracture (Faje et Klibanski, 2012). Given the involvement of CD36 in adipogenesis (Christiaens et al.y 2012) and the reduced fat tissue and body weight of Cd36KO mice, such low body weight may contribute to the reduced bonę mass in Cd36KO mice. To notę, considering that leptin is primarily produced by white adipose tissue, and correlates positively with body fat, reduced fat tissue or lipoatrophy usually associates with low plasma levels of leptin (Haque et al.y 2002). Recently, it has been proposed that peripheral leptin has bonę anabolic effects and contribute to bonę formation (Turner et al.y 2013).

Because of the role attributed to CD36 in the lipid metabolism and due to the possible association of lipid disorders and bonę metabolism, we first determined the cholesterol and lipoprotein profiles of Cd36KO mice. No significant difference was noticed in plasma levels of total cholesterol or cholesterol associated with lipoproteins between Cd36KO and WT mice. Despite the large number of studies on lipid metabolism in Cd36KO mice, the literaturę still reports contradictory results about blood levels of lipids. Several studies have shown increased plasma levels of fasting cholesterol (Brundert et al.y 2011; Febbraio et al.y 1999), non-esterified free fatty acid (Febbraio et al.y 1999; Goudriaan et al.y 2003; Luangrath et al.y 2008) and



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