期刊
BIOMEDICAL AND ENVIRONMENTAL SCIENCES
卷 22, 期 1, 页码 32-39出版社
CHINESE CENTER DISEASE CONTROL & PREVENTION
DOI: 10.1016/S0895-3988(09)60019-2
关键词
Curcumin; Insulin resistance; Inflammation; Adipocyte; Free fatty acids
资金
- Projects in the National Science & Technology Pillar Program
- Industrialization of functional Foods in Reducing Blood Lipid, Pressure and Glucose [2006-2010, 2006BAD27B05]
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 [H-3] 2-deoxyglucose uptake method. Expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by quantitative RT-PCR analysis and ELISA. Nuclear transcription factor kappaB p65 (NF-kappa B 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 cells. Curcumin suppressed the transcription and secretion of TNF-alpha and IL-6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kappa B. The 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 PD99059 or SB203580 (inhibitor of ERK1/2 or p38MAPK, respectively) decreased the up-regulation of TNF-alpha induced by palmitate. Conclusion Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kappa B and JNK pathway.
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