Objective To investigate the attenuating effect of curcumin,an anti-inflammatory compound derived from dietary spice turmeric(Curcuma longa)on the pro-inflammatory insulin-resistant state in 3T3-L1 adipocytes.Methods Glucose uptake rate was determined with the[~3H]2-deoxyglucose uptake method.Expressions of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6) were measured by quantitative RT-PCR analysis and ELISA.Nuclear transcription factor kappaB p65 (NF-κB p65)and mitogen-activated protein kinase(MAPKs)were detected by Western blot assay.Results The basal glucose uptake was not altered,and curcumin increased the insulin-stimulated glucose uptake in 3T3-L1 ceils.Curcumin suppressed the transcription and secretion of TNF-αand IL-6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kB.The activities of Jun NH2-terminal kinase(JNK).extracellular signal-regulated kinasel/2(ERK1/2) and p38MAPK decreased in the presence of curcumin.Moreover,pretreatment with SP600125(inhibitorof JNK)instead of PD98059 or SB203580(inhibitorofERK1/2 or p38MAPK,respectively)decreased the up-regulation of TNF-αinduced by palmitate Conclusion Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kB and JNK pathway. Objective To investigate the attenuating effect of curcumin, an anti-inflammatory compound derived from dietary spice turmeric (Curcuma longa) on the pro-inflammatory insulin-resistant state in 3T3-L1 adipocytes. Methods Glucose uptake rate was determined with the [~ 3H] 2-deoxyglucose uptake method. Expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by quantitative RT-PCR analysis and ELISA. Nuclear transcription factor kappaB p65 Results The basal glucose uptake was not altered, and curcumin increased the insulin-stimulated glucose uptake in 3T3-L1 ceils. Curcumin suppressed the transcription and secretion of TNF-α and IL -6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kB. Activities of Jun NH2-terminal kinase (JNK). Extracellular signal-regulated kinase1 / 2 (ERK1 / 2) and p38MAPK decreased in the presence of curcumin .Moreover, pretreatment with SP600125 (inhibitor of JNK) instead of PD98059 or SB203580 (inhibitor of ERK1 / 2 or p38MAPK, respectively) decreased the up-regulation of TNF-α induced by palmitate Conclusion Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kB and JNK pathway.