HEALTH NEWS

Study Title:

Green Tea Boosts Adiponectin Production by Fat Cells

Study Abstract

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.

Study Information

Si Young Cho, Pil Joon Park, Hyun Jung Shin, Young-Kyung Kim, Dong Wook Shin, Eui Seok Shin, Hyoung Ho Lee, Byeong Gon Lee, Joo-Hyun Baik, and Tae Ryong Lee.
Catechin suppresses expression of Kruppel-like factor 7 and increases expression and secretion of adiponectin protein in 3T3-L1 cells
Am J Physiol Endocrinol Metab
2006 December
Research and Development Center, AmorePacific Corporation, Yongin, Kyeonggi, Korea.