Department of Acupuncture, China Medical University Hospital, Taiwan.
Evid Based Complement Alternat Med. 2011;2011:650263. doi: 10.1093/ecam/neq068. Epub 2011 Feb 14.
Animal studies have shown that electroacupuncture (EA) at Zusanli (ST-36) and Zhongwan (CV-12) acupoints reduces plasma glucose concentrations in rats with type II diabetes. However, whether EA reduces plasma glucose levels in type I diabetes is still unknown. In this study, we explore the various non-insulin-dependent pathways involved in EA-induced lowering of plasma glucose. Streptozotocin (STZ) (60 mg kg(-1), i.v.) was administered via the femoral vein to induce insulin-dependent diabetes in non-adrenalectomized and in adrenalectomomized rats. EA (15 Hz) was applied for 30 min to bilateral ST-36 acupoints after administration of Atropine (0.1 mg kg(-1) i.p.), Eserine (0.01 mg kg(-1) i.p.), or Hemicholinium-3 (5 μg kg(-1) i.p.) in non-adrenalectomized rats. Rats administered acetylcholine (0.01 mg kg(-1) i.v.) did not undergo EA. Adrenalectomized rats underwent EA at bilateral ST-36 acupoints without further treatment. Blood samples were drawn from all rats before and after EA to measure changes in plasma glucose levels. Expression of insulin signaling proteins (IRS1, AKT2) in atropine-exposed rats before and after EA was measured by western blot. Atropine and hemicholinium-3 completely blocked the plasma glucose lowering effects of EA, whereas eserine led to a significant hypoglycemic response. In addition, plasma glucose levels after administration of acetylcholine were significantly lower than the fasting glucose levels. In STZ-adrenalectomized rats, EA did not induce a hypoglycemic response. EA stimulated the expression of IRS1 and AKT2 and atropine treatment blocked the EA-induced expression of those insulin signaling proteins. Taken together, EA at the ST-36 acupoint reduces plasma glucose concentrations by stimulating the cholinergic nerves.
动物研究表明,电针对足三里(ST-36)和中脘(CV-12)穴位的刺激可降低 II 型糖尿病大鼠的血浆葡萄糖浓度。然而,电针是否降低 I 型糖尿病患者的血浆葡萄糖水平仍不清楚。在这项研究中,我们探讨了电针降低血浆葡萄糖所涉及的各种非胰岛素依赖途径。通过股静脉给予链脲佐菌素(STZ)(60mg/kg,静脉注射),在非肾上腺切除和肾上腺切除大鼠中诱导胰岛素依赖型糖尿病。在非肾上腺切除大鼠中,在给予阿托品(0.1mg/kg,腹腔注射)、依色林(0.01mg/kg,腹腔注射)或血卟啉-3(5μg/kg,腹腔注射)后,应用 15Hz 的电针刺激双侧 ST-36 穴位 30 分钟。给予乙酰胆碱(0.01mg/kg,静脉注射)的大鼠不进行电针治疗。肾上腺切除大鼠在双侧 ST-36 穴位进行电针治疗,无需进一步治疗。所有大鼠在电针治疗前后采血,以测量血浆葡萄糖水平的变化。通过 Western blot 测量电针治疗前后阿托品暴露大鼠的胰岛素信号蛋白(IRS1、AKT2)的表达。阿托品和血卟啉-3 完全阻断了电针的降血糖作用,而依色林则导致明显的低血糖反应。此外,给予乙酰胆碱后的血浆葡萄糖水平明显低于空腹血糖水平。在 STZ 肾上腺切除大鼠中,电针不会引起低血糖反应。电针刺激胆碱能神经,从而降低血浆葡萄糖浓度。