Cyanidin 3-glucoside ameliorates hyperglycemia and, insulin sensitivity due to downregulation of retinol binding protein 4 expression in diabetic mice
Cyanidin 3-glucoside ameliorates hyperglycemia and, insulin sensitivity due to downregulation of retinol binding protein 4 expression in diabetic mice
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DOI：
10.1016/j.bcp.2007.08.008
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发表时间：
2007-12-03
影响因子：
5.8
通讯作者：
Tsuda, Takanori
中科院分区：
文献类型：
--
作者：
Sasaki, Rie;Nishimura, Natsumi;Tsuda, Takanori
脂肪细胞功能障碍与肥胖和胰岛素抵抗的发展密切相关。脂肪细胞因子表达的调控是预防肥胖和改善胰岛素敏感性的重要靶点之一。在这项研究中，我们已经证明，花青素（矢车菊素3-葡萄糖苷; C3 G），这是一种广泛存在于植物界的色素，改善高血糖症和胰岛素敏感性，由于减少视黄醇结合蛋白4（RBP 4）的表达在2型糖尿病小鼠。给KK-A（y）小鼠喂食对照或对照+0.2%C3G饮食5周。膳食C3 G显着降低血糖浓度，提高胰岛素敏感性。脂联素及其受体的表达与这种改善无关。C3 G显著上调白色脂肪组织中的葡萄糖转运蛋白4（Glut 4）并下调RBP 4，这伴随着C3 G组的白色脂肪组织中的炎性脂肪细胞因子（单核细胞趋化蛋白-1和肿瘤坏死因子-α）的下调。这些结果表明，C3 G通过调节Glut 4-RBP 4系统和相关的炎性脂肪细胞因子具有显著的抗糖尿病作用。(c)2007爱思唯尔公司All rights reserved.
Adipocyte dysfunction is strongly associated with the development of obesity and insulin resistance. It is accepted that the regulation of adipocytokine expression is one of the most important targets for the prevention of obesity and improvement of insulin sensitivity. In this study, we have demonstrated that anthocyanin (cyanidin 3-glucoside; C3G) which is a pigment widespread in the plant kingdom, ameliorates hyperglycemia and insulin sensitivity due to the reduction of retinol binding protein 4 (RBP4) expression in type 2 diabetic mice. KK-A(y) mice were fed control or control +0.2% of a C3G diet for 5 weeks. Dietary C3G significantly reduced blood glucose concentration and enhanced insulin sensitivity. The adiponectin and its receptors expression were not responsible for this amelioration. C3G significantly upregulated the glucose transporter 4 (Glut4) and downregulated RBP4 in the white adipose tissue, which is accompanied by downregulation of the inflammatory adipocytokines (monocyte chemoattractant protein-1 and tumor necrosis factor-alpha) in the white adipose tissue of the C3G group. These findings indicate that C3G has significant potency in an anti-diabetic effect through the regulation of Glut4-RBP4 system and the related inflammatory adipocytokines. (c) 2007 Elsevier Inc. All rights reserved.