Effects of preventive acupuncture on streptozotocin-induced hyperglycemia in rats.

BACKGROUND: Diabetes prevention has received increasing attention recently. Clinical and experimental studies showed that acupuncture could produce hypoglycemic effect. However, little is known about the effectiveness of acupuncture in diabetes prevention. AIM: To investigate the preventive effects of acupuncture on streptozotocin (STZ)-induced hyperglycemia in rats. METHODS: Hyperglycemia was induced by a single intraperitoneal injection of STZ (60 mg/kg). Rats were randomly divided into six groups (no.=8 each group): control, diabetes, preventive acupuncture plus STZ injection, STZ injection plus therapeutic acupuncture, STZ injection plus preventive and therapeutic acupuncture, and preventive and therapeutic acupuncture control. Body weight, blood glucose, serum insulin, lipid peroxidation, and antioxidant enzymes were measured by routine standard methods. Histological analysis of pancreatic islets was conducted. RESULTS: Preventive acupuncture significantly relieved hyperglycemia, insulin deficiency, weight loss, and pancreatic islet damage in rats with STZ injection; it also significantly reduced serum lipid peroxidation and enhanced superoxide dismutase in the serum and the pancreas without significantly affecting serum glutathione peroxidase and catalase. Therapeutic acupuncture exhibited a hypoglycemic effect in the late stage, but did not significantly improve other parameters. CONCLUSIONS: These results indicate that preventive acupuncture is beneficial to the control of STZ-induced hyperglycemia in rats.

Tumor promotion as a target for estrogen/antiestrogen effects in rat hepatocarcinogenesis.

Tamoxifen is a well-tolerated palliative and adjuvant treatment for human breast cancer and requires continuous, long-term administration for optimal therapeutic effectiveness. A two-stage model of experimental hepatocarcinogenesis, based upon the natural history of cancer development, has been employed to assess the carcinogenic potential of tamoxifen. In this study, the effectiveness of tamoxifen both as an initiator and a promoter in hepatocarcinogenesis was assessed in female F-344 rats. Tamoxifen was tested as an initiator at a single intragastric dose of 40 mg/kg, followed by promotion with 0.05% phenobarbital. The number and size of the resulting altered hepatic lesions were quantified, and tamoxifen was found to lack initiating action at the dose tested. Other groups of animals were initiated with a nonnecrogenic, subcarcinogenic dose of diethylnitrosamine (10 mg/kg) and were fed tamoxifen at either 250 or 500 mg/kg in the AIN-76A purified diet for 6 months. The livers of these animals showed an increase in the size and number of altered hepatic lesions compared with those animals that were initiated but not exposed to tamoxifen; this indicates that tamoxifen acts as a tumor promoter in the rat liver. The promotion index of tamoxifen, a measure of relative potency, was less than one-tenth that of ethinyl estradiol and more than four times that of phenobarbital, an agent commonly employed as a representative promoting agent in experimental carcinogenesis. Since tamoxifen lacked initiating activity in the rat liver at the dose tested, the mechanism of tumor induction in long-term feeding studies by tamoxifen may be due to its promotion of spontaneously initiated hepatocytes. The chronic therapeutic use of tamoxifen should therefore be limited by the potential carcinogenic risk of this agent as an effective tumor promoter.