肥胖是脂肪細胞分裂生長和油脂堆積所造成的常見疾病，會增加癌症、糖尿病、高血壓和心血管疾病的發生。許多研究指出綠茶裡的多酚類，特別是唲茶素，有防止肥胖和其他相關疾病的功能，但是其影響脂肪細胞增生的機制仍未清楚。本研究的第一章指出唲茶素能藉由抑制MEK和其下游Cdk2的活性來減少因胎牛血清所造成的3T3-L1前脂肪細胞增生。第二章則發現唲茶素可以藉由減少第二型類胰島素生長因子接受器與Gi-2蛋白質的結合及下游的MEK活性而阻礙第二型類胰島素生長因子所引起的前脂肪細胞生長。這些研究結果可以提供唲茶素調節許多肥胖模式動物體重的機制。 Obesity, a common disease resulting from mitogenesis and lipid accumulation of fat cells, increases the risks of cancers, diabetes, hypertension, and cardiovascular disease. Based on a variety of laboratory studies, green tea polyphenols, especially the catechin, (-)-epigallocatechin gallate (EGCG), have been proposed as an obesity and other disease chemopreventative. But the exact mechanisms of their action on fat cell mitogenesis are still unclear. Chapter one showed that green tea EGCG could reduce fetal bovine serum-induced mitogenesis of 3T3-L1 preadipocytes through inhibiting the activities of MEK and its downstream cyclin-dependent kinase 2. Chapter two demonstrated that EGCG could stop insulin-like growth factor II (IGF-II)-induced mitogenesis of preadipocytes probably via reducing the IGF-II-stimulated the association of IGF-II receptor with Gi-2 protein and their downstream MEK activity. These results of this thesis provide a mechanism by which EGCG modulates the body weight in various animal models of obesity.
