Intense electroacupuncture normalizes insulin sensitivity, increases muscle GLUT4 content, and improves lipid profile in a rat model of polycystic ovary syndrome. Am J Physiol Endocrinol Metab 299: E551-E559, 2010. First published July 27, 2010; doi:10.1152/ajpendo.00323.2010.-Polycystic ovary syndrome (PCOS) is associated with hyperandrogenism and insulin resistance, possibly reflecting defects in skeletal muscle and adipocyte insulin signaling. Low-frequency (2 Hz) electroacupuncture (EA) increases insulin sensitivity in female rats with dihydrotestosterone (DHT)-induced PCOS, but the mechanism is unclear. We hypothesized that low-frequency EA regulates mediators involved in skeletal muscle glucose uptake and metabolism and alters the lipid profile in rats with DHT-induced PCOS. To test this hypothesis, we implanted in prepubescent female rats 90-day continuousrelease pellets containing DHT (PCOS). At 70 days of age, the rats were randomly subdivided into two groups: one received lowfrequency EA (evoking muscle twitches) for 20 -25 min five times/wk for 4 -5 wk; the other did not. Controls were implanted with pellets containing vehicle only. All three groups were otherwise handled similarly. Lipid profile was measured in fasting blood samples. Insulin sensitivity was determined by euglycemic hyperinsulinemic clamp, soleus muscle protein expression of glucose transporter 4 (GLUT4), and phosphorylated and nonphosphorylated Akt, and Akt substrate of 160 kDa was determined by Western blot analysis and GLUT4 location by immunofluorescence staining. PCOS EA rats had normalized insulin sensitivity, lower levels of total high-density lipoprotein and low-density lipoprotein cholesterol, and increased expression of GLUT4 in different compartments of skeletal muscle compared with PCOS rats. Total weight and body composition did not differ in the groups. Thus, in rats with DHT-induced PCOS, low-frequency EA has systemic and local effects involving intracellular signaling pathways in muscle that may, at least in part, account for the marked improved insulin sensitivity.acupuncture; glucose transporter 4; insulin resistance; muscle contraction; skeletal muscle HYPERANDROGENEMIA IS THE MOST PROMINENT endocrine phenotype in women with polycystic ovary syndrome (PCOS) (56) in addition to ovulatory dysfunction and polycystic ovary morphology (3). The main metabolic phenotype is hyperinsulinemia and insulin resistance, which are independent of body weight (19,40). Other metabolic abnormalities associated with insulin resistance are obesity, dyslipidemia, and increased risk for type 2 diabetes.The mechanisms for the association between endocrine and metabolic abnormalities in PCOS are unclear (13, 18). PCOS is characterized by clinical and/or biochemical hyperandrogenism. In female rats and humans, exogenous exposure to testosterone or dihydrotestosterone (DHT) leads to insulin resistance and obesity (4,14,17,22,50,58). The insulin resistance in women with PCOS is associated with a dyslipidemia characterized by low levels of high...