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Abstract
Furthermore, it has been reported that the surface of cartilage is covered with a layer of phospholipids that serves as a boundary lubricant during joint loading [10]. [...]changes in the composition of this lubrication layer due to either injury or abnormal lipid metabolism may impact the function of the articular joint and potentially lead to the onset of OA [11]. [...]GPR120 stimulation confers protection from obesity and diabetes by inhibiting inflammatory responses, modulating hormone secretions from the gastrointestinal tract and pancreas, and regulating lipid and/or glucose metabolism in adipose, liver, and muscle tissues [15]. In-vitro studies have previously reported that GPR120 signaling negatively regulates osteoclast differentiation, survival, and function [26]. [...]it has also been shown that GPR120 activation-mediated cellular signaling determines the bi-potential of osteogenic and adipogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) in a dose-dependent manner [27]. [...]several in-vivo studies have shown that downregulation of the ω-3-GPR120 signaling leads to abnormalities in bone remodeling or osteophyte formation of subchondral bone in animal model of OA [22, 23].
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