Acupoint-Specific, Frequency-Dependent, and Improved Insulin Sensitivity Hypoglycemic Effect of Electroacupuncture Applied to Drug-Combined Therapy Studied by a Randomized Control Clinical Trial
Table 1
Basic study of the hypoglycemic effect of EA and its influence on insulin activity.
Model categories on different acupoints
Animal models
EA dosage/duration
Conclusion
Reference
EA stimulation at the Zhongwan/Gwanyuan acupoint
Normal rat Neonatal STZ-induced type II diabetic rats Genetically derived type I IDDM rats STZ induced adult type I diabetic rats
15 Hz, 10 mA for 30 min
Electroacupuncture stimulation at the Zhongwan acupoint induces secretion of endogenous -endorphin, which reduces plasma glucose concentrations in an insulin-dependent manner.
Activation of the -opioid receptor by -endorphin secreted from the adrenal gland to release insulin resulting in the decrease of plasma glucose. Mediation of the mu(1) opioid receptor is considered.
Hypoglycemic effect came from adrenal gland, followed by endogenous opioid peptide (EOP) pathway, affected by insulin secretion after 2 Hz EA stimulation at the Zhongwan/Gwanyuan acupoint. Only partial hypoglycemic effect on 2 Hz EA bilateral Zusanli acupoints came from the adrenal gland.
Multiple sources of endogenous opioid peptide participated in the lowering of plasma glucose in rats induced by EA stimulation at higher frequency (15 Hz) at the Zhongwan/Gwanyuan acupoint.
15 Hz EA on bilateral Zusanli acupoints in rats improved glucose tolerance and lowered plasma glucose levels. Hypoglycemic effects of exogenous insulin were enhanced in normal Wistar rats and STZ diabetic rats.
Insulin resistance was successfully induced by a large dose of prednisolone in male rats. This insulin resistance can be improved by 15 Hz EA on the bilateral Zusanli acupoints via decreased plasma levels of FFAs.
STZ-induced insulin dependent non-ADX and ADX diabetic rats
15 Hz, 10 mA for 30 min
15 Hz EA stimulation at the Zusanli acupoints induced a hypoglycemic response in STZ-induced diabetic rats by stimulating the cholinergic nerves and involving the adrenal glands, which in turn stimulates the expression of insulin-signaling proteins.