Fenofibrate enhances CD36 mediated endocytic uptake and degradation of oxidized low density lipoprotein in adipocytes from hypercholesterolemia rabbit

Oxidized LDL impair adipocyte response to insulin by activating serine/threonine kinases

“…OxLDL are considered major players in the pathogenesis of atherosclerosis and have been shown to be greatly increased in the plasma of patients affected by type-2 diabetes, obesity, and metabolic syndrome. In vitro and in vivo experiments seem to suggest interactions between adipocytes and oxLDL as well as a physiological role of adipose tissue in the clearance of circulating oxLDL (51,53,75). In the present study we provide the first evidence that oxLDL induced insulin resistance by impairing insulin signal at multiple levels as shown in Fig.…”

“…Finally, specific receptors for oxLDL, which are active in lipoprotein internalization, have been detected on the membranes of adipocyte cell lines such as 3T3-L1, as well as on human and animal adipocytes (51,52). In particular, the presence of the fatty acid transporter/scavenger receptor CD36, and the oxLDL receptor 1 (ORL1) on adipocytes support the hypothesis that the adipose tissue could be involved in oxLDL metabolism in vivo (53,54). We have recently demonstrated that oxLDL can be actively taken up by 3T3-L1 preadipocytes through a CD36-mediated transport and that they can induce a significant increase in membrane receptor content.…”

Dual effects of oxidized low-density lipoprotein on LXR-ABCA1-apoA-I pathway in 3T3-L1 cells

“…It is now widely accepted that oxidized forms of low-density lipoprotein (LDL) do exist in vivo and at detectable levels in the circulation, even in healthy individuals. Although the role of oxidized LDL (oxLDL) in adipocytes has not been well studied, adipocytes are known to express scavenger receptors, such as scavenger receptor class B type I (SR-BI), CD36 and oxLDL receptor 1 (OLR1), and are capable of uptaking and degrading oxLDL through CD36 and OLR1 [4][5][6]. Increasing evidence suggests that cholesterol balance in adipocytes is an important regulator of metabolic activity and triglyceride storage capability.…”

Soluble epoxide hydrolase inhibitor: A potential target for regulating adipocyte dysfunction

“…As cholesterol cannot be catabolized in adipocytes, multiple pathways are required to extract the excess cholesterol in adipocytes to plasma extracellular acceptor molecules, and these pathways play a crucial role in maintaining cholesterol homeostasis in adipocytes. Our previous studies and the investigations of others have demonstrated that adipocytes from hypercholesterolemic rabbits and 3T3-L1-derived adipocytes have a novel function to uptake and degrade of oxidized low-density lipoprotein (Ox-LDL), via a phagocytic mechanism mediated by CD36 in a similar manner to macrophages [12,13]. When obesity impairs the capability of adipocytes to uptake and degrade Ox-LDL, serum Ox-LDL increases, which in turn promotes the initiation and development of atherosclerotic lesions [14].…”