title: Intense electroacupuncture normalizes insulin sensitivity, increases muscle GLUT4 content, and improves lipid profile in a rat model of polycystic ovary syndrome.
abstract: 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 continuous-release pellets containing DHT (PCOS). At 70 days of age, the rats were randomly subdivided into two groups: one received low-frequency 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.
authors.affiliation: Institute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Julia
authors.initials: J
authors.lastname: Johansson
authors.forename: Yi
authors.initials: Y
authors.lastname: Feng
authors.forename: Ruijin
authors.initials: R
authors.lastname: Shao
authors.forename: Malin
authors.initials: M
authors.lastname: Lönn
authors.forename: Håkan
authors.initials: H
authors.lastname: Billig
authors.forename: Elisabet
authors.initials: E
authors.lastname: Stener-Victorin
mesh_terms: D015670:Acupuncture Therapy / Q000379:methods*; D000818:Animals; D015153:Blotting, Western; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D005455:Fluorescent Antibody Technique; D005947:Glucose / Q000378:metabolism; D015309:Glucose Clamp Technique; D051275:Glucose Transporter Type 4 / Q000378:metabolism*; D015151:Immunoblotting; D007333:Insulin Resistance / Q000502:physiology*; D050356:Lipid Metabolism / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism*; D011085:Polycystic Ovary Syndrome / Q000378:metabolism* / Q000628:therapy*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric; D014280:Triglycerides / Q000097:blood
chemical_list: D051275:Glucose Transporter Type 4; C495694:Slc2a4 protein, rat; D014280:Triglycerides; D002784:Cholesterol; D051057:Proto-Oncogene Proteins c-akt; D005947:Glucose