‣ Close dependence between the risk of aggressive course of RA and leptin levels may exist. ‣ Synovial/serum leptin ratio are correlated with disease duration and parameters of RA activity ‣ Anti-TNF treatment does not affect serum leptin levels. ‣ Leptin increases levels of IL-8 in synovial fibroblast. ‣ Adiponectin levels correlate with disease severity (joint destruction). ‣ Adiponectin may contribute to synovitis and joint destruction ‣ Adiponectin induces IL-6, IL-8, VEGF MMP-1 and MMP-13 by synovial fibroblast ‣ Adiponectin induces COX2, PGES and PGE2 by RA synovial fibroblast. ‣ Contradictory results about anti-TNF treatments effects in adiponectin levels ‣ Resistin levels are higher in RA patients ‣ Anti-TNF-α decreases serum resistin levels ‣ Synovial/Serum levels correlates with inflammatory markers. ‣ Resistin levels increased immediately after joint injury ‣ Visfatin levels are increased in RA patients ‣ Visfatin inhibition reduces arthritis severity and cytokine secretion in a murine model of arthritis ‣ Leptin deficiency induced-obesity does not increase OA risk. ‣ Leptin induces IL-8 and synergize with IL-1 and IFN-gamma to induce Nitric Oxide (NO) in chondrocytes. ‣ Leptin production by OA subchondral osteoblast is increased and involved in altered production of phosphatase alcaline, TGFβ, osteocalcin and collagen I production. ‣ Obese OA chondrocytes have different response to leptin action compared to obese chondrocytes. ‣ Adiponectin levels are increased in OA patients ‣ Adiponectin induces IL-6, IL-8, NO, MCP1 and MMPs by chondrocytes. ‣ Adiponectin synovial levels correlate with OA severity. ‣ Adiponectin levels aree increased in erosive OA. ‣ OA Infra-patellar fat pad has an increased adiponectin production. ‣ Synovial adiponectin/leptin ratio correlates with pain in OA patients  Resistin is elevated in both serum and SF after traumatic joint injuries.  Resistin inhibits proteoglycan synthesis in human cartilage explants. ‣ Visfatin expression is increased in OA chondrocytes ‣ IL1-β increases visfatin production by human OA chondrocytes ‣ Visfatin induces the expression of MMPs and reduces matrix components synthesis  Leptin, and high fat diet, are able to induce pro-inflammatory high- density iIpoproteins and atherosclerosis in BWF1 lupus prone mice.  Patients with SLE have increased concentrations of leptin and these concentrations are associated with insulin resistance, BMI (Body Mass Index) and CRP (C-reactive protein) in these patients.  Adiponectin serum levels are increased in SLE patients comparison with healthy controls. Among the SLE patients, patients with insulin resistance (IR) showed significantly lower adiponectin levels than patients without IR  Adiponectin levels are increased in patients with renal SLE compared to healthy controls and patients with non- renal SLE.  Positive correlation between serum resistin levels, inflammation, bone mineral density and renal functions in patients with SLE.  Visfatin levels were higher in SLE patients compared to healthy controls. LEPTINADIPONECTIN RESISTIN RA OA SLE VISFATIN

 IL-1 β is a potent inducer of chemerin, LCN2 and SAA3 expression in chondrocytes.  Dexamethasone induces expression of LCN2 and chemerin in chondrocytes.  LPS induces the expression of LCNN2 and SAA3 in chondrocytes.  Chemerin, LCN2 and SAA3 expression are temporally regulated during chondrogenic differentiation.  Leptin and adiponectin modulate LCN2 and SAA3 expression in chondrocytes  In chondrocytes LCN2 forms a complex with MMP9 protecting this MMP by auto-degradation.  Human analogue of SAA3 can induce MMPs synthesis in human chondrocytes. CHEMERIN LIPOCALIN 2 SAA3 ARTICULAR ACTIVITIES APELIN VASPIN OMENTIN  Apelin stimulates the proliferation of chondrocytes and significantly increases mRNA levels of MMP-1, -3, -9 and IL-1β in vitro. Intra-articular injection with apelin in vivo up-regulates the expression of MMP-3, -9, and IL-1β as well as decreases the level of collagen II.  Levels of vaspin are increased in the synovial fluid of patients with RA compared with those with OA.  Levels of omentin are reduced in the synovial fluid of patients with RA compared with those with OA.