[Effects of electroacupuncture intervention on expression of hypothalamic PI 3 K and p-PI 3 K Proteins in insulin resistance model rats]

Abstract

Objective: To observe the effect of "Shuanggu Yitong" (Double-reinforcing and one-unblocking) needling [electroacupuncture (EA) of "Guanyuan" (CV 4), "Housanli" (ST 36), "Fenglong" (ST 40) and "Zhongwan" (CV 12)] on expression of hypothalamic phosphatidylinositol 3-kinase (PI 3 K) and p-PI 3 K proteins in insulin resistance rats.

Methods: Sixty Wistar rats were randomized into normal control, model, EA prevention, EA, cerebrospinal fluid (CSF), and Wortmannin (PI 3 K antagonist) groups (n = 10 rats/group). Insulin resistance model was established by feeding the animal with high fat forage continuously for 8 weeks. For rats of the EA group, EA (2 Hz, 1 mA) was applied to ipsilateral "Housanli"(ST 36)-"Fenglong" (ST 40), and "Guanyuan" (CV 4)-"Zhongwan" (CV 12) for 15 min, once daily, 5 times a week and for 8 weeks, beginning after modeling. For rats of the EA prevention group, EA was conducted simultaneously with the modeling. For rats of the Wortmannin group and CSF group, cerebroventricular microinjection of Wortmannin (50 nmol/L, 3 mg/kg) or artificial CSF was given through an implanted steel cannel. Fasting plasma glucose (FPG) and fasting serum insulin (FINS) contents were assayed using glucose-tested instrument and ELISA respectively, insulin activity index (IAI) was calculated [IAI = Ln (1/FPG x FINS)], and the expres- sion of hypothalamic PI 3 K and p-PI 3 K proteins was detected by Western blot.

Results: In comparison with the normal control group, the body weight (BW), FPG and FINS contents at time-points of 8 and 16 weeks were considerably increased (P < 0.01), and IAI, hypothalamic PI 3 Kp 110 and p-PI 3 Kp 110 protein expression levels were obviously decreased in the model group (P < 0.01). Compared with the model group, the FPG and FINS contents at the 8th week after modeling in the EA prevention group, the BW and FPG levels at the 16th week in the EA prevention, EA and CSF groups, FINS levels at the 16th week in the EA prevention and EA groups were remarkably decreased (P<0.05, P<0.01), IAI, and hypothalamic PI 3 Kp 110 and p-PI 3 Kp 110 protein expression levels were significantly up-regulated in the EA prevention, EA and CSF groups (P < 0.05, P < 0.01). No significant differences were found among the EA prevention, EA and CSF groups, and between the model and Wortmannin groups in the BW, FPG, FINS, IAI and hypothalamic PI 3 Kp 110 and p-PI 3 Kp 110 expression levels (P > 0.05).

Conclusion: EA intervention can reduce insulin resistance by suppressing the increase of body weight, blood glucose and insulin contents, and increasing hypothalamic PI 3 K expression levels in insulin resistance rats.