ABSTRACT
Objective : We examined the effects of acupuncture stimulation on hyper lipidemia induced by a cholesterol-free, high-fructose diet (HFD) in rats.<BR>Methods : Acupoints on the rats' bodies were selected at the positions relative to the human acupoints, such as BL 18, LR 14, CV 12, ST 36 and T13-L1, which starts of the origin of splanchnic nerve and runs at intervals of 1 cm on both sides of the nerve between the spinous process of the thirteenth thoracic vertebra and the first lumber vertebra (T13-L1). Nonacupoints were selected on bi lateral buttocks for rats fed with a normal diet and HFD control. Acupuncture stimulations were administered by the subcutaneous insertion of acus. The stimulation was started with HFD feeding and continued for two weeks.<BR>Results : Feeding with HFD for 2 weeks incresed the levels of total cholesterol (TC), especially in very low density lipoprotein (VLDL) and low density lipoprotein (LDL), free cholesterol (FC), triglyceride (TG) and phospholipiid (PL) in serum. Acupuncture stimulations of BL18, LR14, CV12 and S36 inhibited the increase of TC, while the increase of VLDL·LDL-C was inhibited by the acupuncture stimulation of all acupoints. The stimulation of BL18, LR14 and ST36 inhibited the increase of FC. The stumulation of T13-L1 inhibited the increases of TG, TG in high density lipoprotein and PL. The increase of TG in liver by HFD feeding was inhibited by the stimulations on LR14, T13-L1 and CV 12. The reductions of glucose-6-phosphate dehydrogenase and malic enzyme activities in the liver of rats fed by HFD feeding were enhanced by the stimulation of T13-L1 and S36. The activity of β-oxdation in the liver was slightly increased by the stimulations on LR14 and ST36.<BR>Conclusions : These results suggest that the acupuncture stimulation on BL18, LR14, CV12 and ST36 inhibited the increase of intrinsic cholesterol and enhanced the metabolism of VLDL·LDL-C. In addition, it appears that the mechanism of TG decrease by the stimulation on LR14, T13-L1 and ST36 was related to the inhibition of fatty acid synthesis and the enhancement of fatty acid metabolism in the liver.