Beltsville Human Nutrition Research Center, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705, USA.
J Nutr Biochem. 2009 Nov;20(11):901-8. doi: 10.1016/j.jnutbio.2008.08.005. Epub 2008 Nov 6.
We have reported previously that a cinnamon extract (CE), high in type A polyphenols, prevents fructose feeding-induced decreases in insulin sensitivity and suggested that improvements of insulin sensitivity by CE were attributable, in part, to enhanced insulin signaling. In this study, we examined the effects of CE on postprandial apolipoprotein (apo) B-48 increase in fructose-fed rats, and the secretion of apoB48 in freshly isolated intestinal enterocytes of fructose-fed hamsters. In an olive oil loading study, a water-soluble CE (Cinnulin PF, 50 mg/kg body weight, orally) decreased serum triglyceride (TG) levels and the over production of total- and TG-rich lipoprotein-apoB48. In ex vivo (35)S labeling study, significant decreases were also observed in apoB48 secretion into the media in enterocytes isolated from fructose-fed hamsters. We also investigated the molecular mechanisms of the effects of CE on the expression of genes of the insulin signaling pathway [insulin receptor (IR), IR substrate (IRS)1, IRS2 and Akt1], and lipoprotein metabolism [microsomal TG transfer protein (MTP), sterol regulatory element-binding protein (SREBP1c) in isolated primary enterocytes of fructose-fed hamsters, using quantitative real-time polymerase chain reaction. The CE reversed the expression of the impaired IR, IRS1, IRS2 and Akt1 mRNA levels and inhibited the overexpression of MTP and SREBP1c mRNA levels of enterocytes. Taken together, our data suggest that the postprandial hypertriglycerides and the overproduction of apoB48 can be acutely inhibited by a CE by a mechanism involving improvements of insulin sensitivity of intestinal enterocytes and regulation of MTP and SREBP1c levels. We present both in vivo and ex vivo evidence that a CE improves the postprandial overproduction of intestinal apoB48-containing lipoproteins by ameliorating intestinal insulin resistance and may be beneficial in the control of lipid metabolism.
我们之前曾报道过，一种富含 A 型多酚的肉桂提取物（CE）可预防果糖喂养引起的胰岛素敏感性降低，并表明 CE 对胰岛素敏感性的改善部分归因于胰岛素信号的增强。在这项研究中，我们研究了 CE 对果糖喂养大鼠餐后载脂蛋白（apo）B-48 增加的影响，以及果糖喂养仓鼠新鲜分离的肠上皮细胞中 apoB48 的分泌。在橄榄油负荷研究中，一种水溶性 CE（Cinnulin PF，50mg/kg 体重，口服）降低了血清甘油三酯（TG）水平和总 TG 丰富脂蛋白 apoB48 的过度产生。在离体（35）S 标记研究中，还观察到从果糖喂养的仓鼠分离的肠上皮细胞中 apoB48 分泌到培养基中的显著减少。我们还研究了 CE 对胰岛素信号通路基因（胰岛素受体（IR）、IR 底物（IRS）1、IRS2 和 Akt1）和脂蛋白代谢基因（微粒体 TG 转移蛋白（MTP）、固醇调节元件结合蛋白（SREBP1c）的表达的影响的分子机制，在果糖喂养的仓鼠的分离的原代肠上皮细胞中，使用定量实时聚合酶链反应。CE 逆转了受损的 IR、IRS1、IRS2 和 Akt1 mRNA 水平的表达，并抑制了肠上皮细胞中 MTP 和 SREBP1c mRNA 水平的过度表达。综上所述，我们的数据表明，CE 可以通过改善肠上皮细胞的胰岛素敏感性和调节 MTP 和 SREBP1c 水平的机制，急性抑制餐后高甘油三酯血症和 apoB48 的过度产生。我们提供了体内和离体证据，表明 CE 通过改善肠胰岛素抵抗来改善餐后肠 apoB48 含脂蛋白的过度产生，并且可能有益于控制脂质代谢。
