結果：
由實驗結果發現STZ糖尿病大鼠給予Eserine（0.01 mg/kg i.p.）30分鐘後，以15 Hz電針足三里穴可提升血糖下降程度，acetylcholine大量增加與血糖下降呈正相關；直接給與acetylcholine藥物後，其實驗結果為STZ糖尿病大鼠給予Acetylcholine（0.01 mg/kg i.v.）後測量血糖值，血糖在60分鐘時與未給Acetylcholine空腹血糖相比，有顯著差異。15 Hz電針STZ糖尿病大鼠足三里穴，30分鐘後可被Hemicholine-3（5 ug/kg i.p.）阻斷其降血糖的作用。15 Hz電針STZ去腎上腺糖尿病大鼠足三里穴，發現電針STZ去腎上腺大鼠其降血糖的作用被阻斷。
電針加強STZ糖尿病大鼠ICT降糖作用，可藉由副交感神經之活化，而加強了胰島素的敏感度與胰島素訊息之傳遞有關。
結論：
本研究的主要目的是藉由第一型的糖尿病動物模式進一步探討15Hz電針足三里穴在胰島素依賴降血糖作用之機轉。研究結果發現此一電針可透過副交感神經與腎上腺的調節，而達到降低第一型的糖尿病大鼠動物模式血糖的目的。進一步探討電針加強胰島素的降血糖功效，藉由先前的電針增強糖耐量探討中發現，其機轉與體內副交感神經的活性有關。
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 (15Hz) was applied for 30min to bilateral ST-36 acupoints after administration of Atropine (0.1 mg kg-1 i.p.), Eserine (0.01mg kg−1 i.p.), or Hemicholinium-3 (5 μg kg-1 i.p.) in nonadrenalectomized rats. Rats administered acetylcholine (0.01mg 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.
