Abstract
In rats with 2-deoxy-2-(3-(methyl-3-nitrosoureido)-d-glucopyranose streptozotocin- (STZ-) induced insulin-dependent diabetes (IDDM), continuous 15 Hz electrical stimulation at bilateral ST36 acupoints for 30 and 60 minutes has been shown to prevent hyperglycemia. We hypothesized that the mechanism of action in STZ-induced IDDM rats is that electrical stimulation at bilateral ST36 acupoints is effective in improving insulin receptor substrate type 1 (IRS-1) and glucose transporter type 4 (GLUT4) protein expressions associated with counteracting both plasma glucose and free fatty acid (FFA) levels during isoflurane anesthesia. In this study, twenty-six healthy male Wistar rats, weighing 250–350 g and aged 8–10 weeks were tested. Rats in the experimental electroacupuncture (EA) group (n = 13) received 15 Hz electrical stimulation at bilateral ST 36 acupoints for 30 and 60 minutes. Rats in the control group (n = 13) were handled but not subjected to the stimulation treatment. In both IDDM and normal Wistar rats, we observed a negative change in plasma glucose levels when rats were given the EA treatment, but a positive change in plasma glucose without EA treatment relative to baseline. Within the IDDM group, a negative change in FFA levels was observed when rats were given the EA treatment, while a positive change in the FFA level was shown without the EA treatment. In the expressed protein signals, we found a significant elevation in both GLUT4 and IRS-1 proteins in the IDDM group treated by EA. Moreover, we found a significant mean difference between GLUT4 and IRS-1 protein expression levels relative to β-actin. Our findings suggested that EA at bilateral ST36 acupoints could serve as an effective strategy for lowering plasma glucose by decreasing free fatty acid levels and improving the expression of IRS-1 and GLUT4 proteins in a STZ-IDDM rat model during isoflurane anesthesia.
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