(-)-Catechin suppresses expression of Kruppel-like factor 7 and increases expression and secretion of adiponectin protein in 3T3-L1 cells

• Published in: American journal of physiology: endocrinology and metabolism Vol. 292; no. 4; pp. E1166 - E1172
• Main Authors: 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
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.04.2007
• Subjects: 3T3-L1 Cells; Adenoviridae - genetics; Adipocytes - cytology; Adipocytes - drug effects; Adipocytes - metabolism; Adipogenesis - drug effects; Adiponectin - metabolism; Adiponectin - pharmacology; Adiponectin - secretion; Animals; Body fat; Catechin - administration & dosage; Catechin - pharmacology; Cell Differentiation; Cells; Dose-Response Relationship, Drug; Drug Synergism; Fatty acids; Gene expression; Gene Transfer Techniques; Genes; Genetic Vectors; Glucose - pharmacokinetics; Hormones; Humans; Insulin - pharmacology; Kruppel-Like Transcription Factors - antagonists & inhibitors; Kruppel-Like Transcription Factors - genetics; Mice; Proteins; Rodents; Tea
• ISSN: 0193-1849; 1522-1555
• DOI: 10.1152/ajpendo.00436.2006

Research and Development Center, AmorePacific Corporation, Yongin, Kyeonggi, Korea Submitted 22 August 2006 ; accepted in final form 10 December 2006 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 PPAR , CEBP , 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, PPAR , C/EBP , 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. Address for reprint requests and other correspondence: T. R. Lee, R&D Center, AmorePacific Corp., 314-1, Bora-dong, Giheung-gu, Yongin-si, Gyeonggi-do, 449-729, Korea (e-mail: trlee{at}amorepacific.com )