United States Department of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center, Diet, Genomics and Immunology Laboratory, Beltsville, Maryland, USA.
Nutrition. 2012 Nov-Dec;28(11-12):1172-9. doi: 10.1016/j.nut.2012.03.020. Epub 2012 Aug 2.
Increasing evidence suggests that dietary factors may affect the expression of multiple genes and signaling pathways, which regulate intestinal lipoprotein metabolism. The small intestine is actively involved in the regulation of dietary lipid absorption, intracellular transport, and metabolism and is closely linked to systemic lipid metabolism. Cinnamon polyphenols have been shown to improve glucose, insulin, and lipid metabolism and improve inflammation in cell culture, animal, and human studies. However, little is known of the effects of an aqueous cinnamon extract (CE) on the regulation of genes and signaling pathways related to intestinal metabolism. The aim of the study was to investigate the effects of a CE on the primary enterocytes of chow-fed rats.
Freshly isolated intestinal enterocytes were used to investigate apolipoprotein-B48 secretion by immunoprecipitation; gene expressions by quantitative reverse transcriptase-polymerase chain reaction and the protein and phosphorylation levels were evaluated by western blot and flow cytometric analyses.
Ex vivo, the CE significantly decreased the amount of apolipoprotein-B48 secretion into the media, inhibited the mRNA expression of genes of the inflammatory cytokines, interleukin-1β, interleukin-6, and tumor necrosis factor-α, and induced the expression of the anti-inflammatory gene, Zfp36. CE also increased the mRNA expression of genes leading to increased insulin sensitivity, including Ir, Irs1, Irs2, Pi3k, and Akt1, and decreased Pten expression. CE also inhibited genes associated with increased cholesterol, triacylglycerols, and apolipoprotein-B48 levels, including Abcg5, Npc1l1, Cd36, Mttp, and Srebp1c, and facilitated Abca1 expression. CE also stimulated the phospho-p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, and extracellular-signal-regulated kinase expressions determined by flow cytometry, with no changes in protein levels.
These results demonstrate that the CE regulates genes associated with insulin sensitivity, inflammation, and cholesterol/lipogenesis metabolism and the activity of the mitogen-activated protein kinase signal pathway in intestinal lipoprotein metabolism.
越来越多的证据表明，饮食因素可能影响调节肠道脂蛋白代谢的多个基因和信号通路的表达。小肠积极参与调节膳食脂质吸收、细胞内转运和代谢，并与全身脂质代谢密切相关。肉桂多酚已被证明可改善细胞培养、动物和人体研究中的葡萄糖、胰岛素和脂质代谢，并改善炎症。然而，人们对水提肉桂提取物（CE）对与肠道代谢相关的基因和信号通路调节的影响知之甚少。本研究旨在探讨 CE 对正常饮食大鼠原代肠细胞的影响。
使用新鲜分离的肠上皮细胞通过免疫沉淀法研究载脂蛋白 B48 的分泌；通过定量逆转录聚合酶链反应和蛋白质及磷酸化水平的 Western blot 和流式细胞分析评估基因表达。
离体时，CE 显著减少载脂蛋白 B48 分泌到培养基中的量，抑制促炎细胞因子白细胞介素 1β、白细胞介素 6 和肿瘤坏死因子-α的基因表达，并诱导抗炎基因 Zfp36 的表达。CE 还增加了与胰岛素敏感性增加相关的基因的表达，包括 Ir、Irs1、Irs2、Pi3k 和 Akt1，并降低了 Pten 的表达。CE 还抑制了与胆固醇、三酰甘油和载脂蛋白 B48 水平升高相关的基因，包括 Abcg5、Npc1l1、Cd36、Mttp 和 Srebp1c，并促进 Abca1 的表达。CE 还通过流式细胞术刺激磷酸化 p38 丝裂原激活蛋白激酶、c-Jun N 端激酶和细胞外信号调节激酶的表达，而蛋白质水平没有变化。
这些结果表明，CE 调节与胰岛素敏感性、炎症和胆固醇/脂肪生成代谢以及肠道脂蛋白代谢中丝裂原激活蛋白激酶信号通路活性相关的基因。
