Ethanolic Extract of Fermented Brown Rice Improves the Metabolism of Glucose and Lipids in 3T3-L1 Adipocytes
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Abstract:
The effects of fermented brown rice ethanolic extracts (FBREE) on glucose and lipid metabolism in insulin-resistant 3T3-L1 adipocytes were investigated. The insulin-resistant model cells were established through the induction by high glucose concentration together with high insulin. The model cells were treated with different concentrations of FBREE for 24 h, and the levels of glucose, free fatty acid (FFA), glycerol, triglyceride (TG), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the culture medium were determined. The mRNA expression levels of peroxisome proliferator-activated receptors γ (PPARγ), CAATT enhancer binding proteins α (C/EBPα), sterol regulatory element binding protein1c (SREBP1c), adipocyte fatty acid binding protein 2(aP2), protein tyrosine phosphatase-1B (PTP1B), glucose transporter 4 (GLUT4), hormone-sensitive triglyceride lipase (HSL), TNF-α, IL-6, monocyte chemotactic protein (MCP)-1 and C-reaction protein (CRP) were determined by quantitative real-time PCR (qRT-PCR) assay. FBREE could promote cellular glucose utilization, decrease the cellular TG content and reduce the released FFA and glycerol in model cells. The high dose of FBREE (100 μg/mL) reduced the cellular TG (by 52.44%) and FFA (by 37.83%), compared with those of the model cells. FBREE also reduced the TNF-α and IL-6 secretion in model cells. A high dose of FBREE (100 μg/mL) also reduced the mRNA expression levels of TNF-α (by 21.18%)，IL-6 (by 31.39%)，MCP-1 (by 40.09%) and CRP (by 41.73%) compared with those in model cells. In addition, FBREE was able to reduce effectively the mRNA expressions of PPARγ, C/EBPα，SREBP1c, PTP1B, aP2 and HSL, while up-regulating the mRNA levels of GLUT4. These results suggested that the FBREE treatment can promote effectively glucose consumption, TG decomposition, and reduction of FFA and glycerol release, as well as regulate the glucose and lipid metabolism to ameliorate insulin resistance and reduce the increase of inflammation caused by insulin resistance.
