Objective: To investigate the effects of green tea polysaccharides (TPs) on glucose metabolism and the activity of peroxisome proliferator-activated receptor gamma (PPAR-?) in KKAy type 2 diabetic mice. Methods: Glucose tolerance test, fasting and postprandial glucose, gluconeogenesis, and insulin sensitivity were investigated in type 2 diabetic mice with orally administered TPs at the dose of 500mg/kg for 4-10 w. Effect of TPs on activity of PPAR-? was tested in vitro. Results: TPs could not only improve glucose tolerance, but also reduce fasting and postprandial blood glucose. In addition, TPs could inhibit gluconeogenesis and enhance insulin sensitivity in KKAy diabetic mice. TPs had also an effect of activating of PPAR-? with dose-response. Conclusion: TPs have beneficial effect of lowering blood glucose in KKAy type 2 diabetic mice, which may be induced by enhancing insulin sensitivity by activating of PPAR-?.

Objective: To investigate how fatty liver was developed in ventromedial hypothalamus(VMH)-lesioned obese rats. Methods: Two groups of rats were prepared: (1)VMH-lesioned obese rats, and (2)sham VMH-lesioned rats. One week after VMH lesions, livers of all rats were isolated for morphological observation and for determination of microsomal triglyceride transfer protein(MTP), phosphatidate phyosphohydrolase (PAP), malic enzyme (ME), and glucose-6-phosphate dehydrogenase(G6PDH). Results: Triglyceride contents in livers of VMH-lesoned obese rats increased significantly, and were about 1.8-fold of control group. Activities of ME, G6PDH and PAP in the livers were also enhanced markedly compared to their controls. Many lipid droplets in cytoplasm of hepatocytes from VMH-lesioned obese rats were observed, while there was no similar finding in hepatocytes of control rats. MTP activity in livers of VMH-lesioned obese rats was higher than that in livers of sham-operated non-obese rats [0.201?0.013 vs. 0.175?0.014 ?g/(mg protein?h),[WTBX]P0.05). Conclusion: Hepatic triglyceride production and activity of MTP were increased in VMH-lesioned obese rats, but magnitude of the latter did not exceed the former. This resulted in hepatic triglyceride accumulation in spite of increase in transport of triglyceride out of liver by MTP. This may contribute to the development of fatty liver in VMH-lesioned obese rats.