Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, US Department of Agriculture, Beltsville, Maryland 20705, USA.
Horm Metab Res. 2010 Mar;42(3):187-93. doi: 10.1055/s-0029-1242746. Epub 2009 Nov 23.
We reported earlier that dietary cinnamon extract (CE) improves systemic insulin sensitivity and dyslipidemia by enhancing insulin signaling. In the present study, we have examined the effects of CE on several biomarkers including plasma levels of adipose-derived adipokines, and the potential molecular mechanisms of CE in epididymal adipose tissue (EAT). In Wistar rats fed a high-fructose diet (HFD) to induce insulin resistance, supplementation with a CE (Cinnulin PF, 50 mg/kg daily) for 8 weeks reduced blood glucose, plasma insulin, triglycerides, total cholesterol, chylomicron-apoB48, VLDL-apoB100, and soluble CD36. CE also inhibited plasma retinol binding protein 4 (RBP4) and fatty acid binding protein 4 (FABP4) levels. CE-induced increases in plasma adiponectin were not significant. CE did not affect food intake, bodyweight, and EAT weight. In EAT, there were increases in the insulin receptor ( IR) and IR substrate 2 ( IRS2) mRNA, but CE-induced increases in mRNA expression of IRS1, phosphoinositide-3-kinase, AKT1, glucose transporters 1 and 4 , and glycogen synthase 1 expression and decreased trends in mRNA expression of glycogen synthase kinase 3beta were not statistically significant. CE also enhanced the mRNA levels of ADIPOQ, and inhibited sterol regulatory element binding protein-1c mRNA levels. mRNA and protein levels of fatty acid synthase and FABP4 were inhibited by CE and RBP4, and CD36 protein levels were also decreased by CE. These results suggest that CE effectively ameliorates circulating levels of adipokines partially mediated via regulation of the expression of multiple genes involved in insulin sensitivity and lipogenesis in the EAT.
我们之前曾报道过,膳食肉桂提取物(CE)通过增强胰岛素信号来改善全身胰岛素敏感性和血脂异常。在本研究中,我们研究了 CE 对几种生物标志物的影响,包括血浆脂肪细胞因子水平,以及 CE 对附睾脂肪组织(EAT)的潜在分子机制。在给予高果糖饮食(HFD)诱导胰岛素抵抗的 Wistar 大鼠中,补充 CE(Cinnulin PF,每天 50mg/kg)8 周可降低血糖、血浆胰岛素、甘油三酯、总胆固醇、乳糜微粒-载脂蛋白 B48、VLDL-载脂蛋白 B100 和可溶性 CD36。CE 还抑制血浆视黄醇结合蛋白 4(RBP4)和脂肪酸结合蛋白 4(FABP4)水平。CE 诱导的血浆脂联素增加不显著。CE 不影响食物摄入量、体重和 EAT 重量。在 EAT 中,胰岛素受体(IR)和 IR 底物 2(IRS2)mRNA 增加,但 CE 诱导的 IRS1、磷酸肌醇 3-激酶、AKT1、葡萄糖转运蛋白 1 和 4 以及糖原合酶 1 的 mRNA 表达增加,糖原合酶激酶 3beta 的 mRNA 表达呈下降趋势,但无统计学意义。CE 还增强了 ADIPOQ 的 mRNA 水平,并抑制了固醇调节元件结合蛋白-1c 的 mRNA 水平。CE 抑制了脂肪酸合酶和 FABP4 的 mRNA 和蛋白水平,RBP4 和 CD36 蛋白水平也降低。这些结果表明,CE 通过调节参与胰岛素敏感性和脂肪生成的多个基因的表达,有效改善了循环脂肪细胞因子水平。