Feier Cheng,Xinhui Ge,Yao Zhang,Jia Li,Shaoqing Yan,Yunlong Li,Min Wang
The hypoglycemic effects and underlying molecular mechanisms of combining two dietary compounds, quercetin (Que) and d-chiro-inositol (DCI) on hepatic insulin resistance in C57BL/6J mice that were fed a high fat diet and saturated palmitic acid (PA)-treated hepatocytes were studied. Catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) are important antioxidant enzymes . Insufficient secretion of these enzymes will inhibit the normal phosphorylation of insulin receptors in the liver, thereby limiting the transmission of insulin signals and producing insulin resistance. The results showed that QD (both Que and DCI) led to the recovery of the activity of CAT, SOD, GPx, suggesting that QD was helpful in preventing mice hepatic insulin resistance. In PA-induced human hepatoma cells (HepG2), QD improved the antioxidant level in cells. The fluoro-immunoassay showed that QD effectively reduced the translocation of protein kinase Cε to cell membranes in the HepG2. Western blotting results suggested that QD increased the signal transduction in the IRS-2/PI3K/Akt/FoxO1 pathway. Overall, these results showed that the combination of 5 μmol Que and 5 μmol DCI ameliorated high fat diet-induced hepatic insulin resistance.
Jiarui Nie,Yaning Chang,Yujia Li,Yingjun Zhou,Jiawen Qin,Zhen Sun,Haibin Li
Caffeic acid phenethyl ester (CAPE), extracted from propolis, was evaluated for the ameliorative effects on insulin resistance and the mechanisms were identified, using non-insulin-dependent diabetes mellitus (NIDDM) model mice and insulin resistance (IR) model cells. After 5 weeks of CAPE supplementation, insulin sensitivity, hyperlipidemia, and peroxisome proliferator-activated receptor-α (PPAR-α) levels were improved in mice. Proinflammatory cytokines in serum and the expressions of tumor necrosis factor-alpha (TNF-α) mRNA in tissues were markedly downregulated from CAPE-treated mice. In vitro, CAPE supplement significantly improved glucose consumption, glucose uptake, glycogen content, and oxidative stress and decreased expression of glucose-6-phosphatase (G6Pase) mRNA in cells. Both in vivo and in vitro, CAPE enhanced p-Akt (Ser473) and p-insulin receptor substrate (IRS)-1 (Tyr612), but inhibited p-JNK (Thr183/Tyr185), p-NF-κB p65 (Ser536), and nuclear translocation of p-NF-κB p65 (Ser536). In summary, CAPE can ameliorate insulin resistance through modulation of JNK and NF-κB signaling pathway in mice and HepG2 cells.
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