Cho Si Young, Park Pil Joon, Shin Hyun Jung, Kim Young-Kyung, Shin Dong Wook, Shin Eui Seok, Lee Hyoung Ho, Lee Byeong Gon, Baik Joo-Hyun, Lee Tae Ryong
Research and Development Center, AmorePacific Corporation, 314-1, Bora-dong, Giheung-gu, Yongin-si, Gyeonggi-do, 449-729, Korea.
Am J Physiol Endocrinol Metab. 2007 Apr;292(4):E1166-72. doi: 10.1152/ajpendo.00436.2006. Epub 2006 Dec 12.
Adiponectin is an adipocyte-specific secretory hormone that can increase insulin sensitivity and promote adipocyte differentiation. Administration of adiponectin to obese or diabetic mice reduces plasma glucose and free fatty acid levels. Green tea polyphenols possess many pharmacological activities such as antioxidant, anti-inflammatory, antiobesity, and antidiabetic activities. To investigate whether green tea polyphenols have an effect on the regulation of adiponectin, we measured expression and secretion levels of adiponectin protein after treatment of each green tea polyphenols in 3T3-L1 adipocytes. We found that (-)-catechin enhanced the expression and secretion of adiponectin protein in a dose- and time-dependent manner. Furthermore, treatment of (-)-catechin increased insulin-dependent glucose uptake in differentiated adipocytes and augmented the expression of adipogenic marker genes, including PPARgamma, CEBPalpha, FAS, and SCD-1, when (-)-catechin was treated during adipocyte differentiation. In search of the molecular mechanism responsible for inducible effect of (-)-catechin on adiponectin expression, we found that (-)-catechin markedly suppresses the expression of Kruppel-like factor 7 (KLF7) protein, which has recently been reported to inhibit the expression of adiponectin and other adipogenesis related genes, including leptin, PPARgamma, C/EBPalpha, and aP2 in adipocytes. KLF7 is a transcription factor in adipocyte and plays an important role in the pathogenesis of type 2 diabetes. Taken together, these data suggest that the upregulation of adiponectin protein by (-)-catechin may involve, at least in part, suppression of KLF7 in 3T3-L1 cells.
脂联素是一种脂肪细胞特异性分泌激素,可提高胰岛素敏感性并促进脂肪细胞分化。给肥胖或糖尿病小鼠注射脂联素可降低血浆葡萄糖和游离脂肪酸水平。绿茶多酚具有多种药理活性,如抗氧化、抗炎、抗肥胖和抗糖尿病活性。为了研究绿茶多酚是否对脂联素的调节有影响,我们在3T3-L1脂肪细胞中用每种绿茶多酚处理后,测量了脂联素蛋白的表达和分泌水平。我们发现(-)-表儿茶素以剂量和时间依赖性方式增强了脂联素蛋白的表达和分泌。此外,当在脂肪细胞分化过程中用(-)-表儿茶素处理时,(-)-表儿茶素处理增加了分化脂肪细胞中胰岛素依赖性葡萄糖摄取,并增强了包括PPARγ、CEBPα、FAS和SCD-1在内的脂肪生成标记基因的表达。在寻找(-)-表儿茶素对脂联素表达诱导作用的分子机制时,我们发现(-)-表儿茶素显著抑制Kruppel样因子7(KLF7)蛋白的表达,最近有报道称该蛋白可抑制脂肪细胞中脂联素和其他脂肪生成相关基因(包括瘦素、PPARγ、C/EBPα和aP2)的表达。KLF7是脂肪细胞中的一种转录因子,在2型糖尿病的发病机制中起重要作用。综上所述,这些数据表明(-)-表儿茶素对脂联素蛋白的上调可能至少部分涉及对3T3-L1细胞中KLF7的抑制。