title: Muscle insulin receptor concentrations in obese patients post bariatric surgery: relationship to hyperinsulinemia.
abstract: OBJECTIVE
  Obesity results in insulin resistance. Bariatric surgery for obese individuals induces weight loss, improves insulin sensitivity, and lowers insulin levels. We investigated the mechanisms of this improvement.
  
  
  METHODS
  Insulin receptor (IR) content, IR signaling, and adiponectin levels were measured in nine morbidly obese subjects before and after bariatric surgery.
  
  
  METHODS
  Seven female and two male, average age 44+/-2y, BMI >40 kg/m(2) and/or at least 100 lbs over ideal body weight, undergoing elective bariatric surgery.
  
  
  METHODS
  Before surgery BMI, fasting plasma glucose, adiponectin, and insulin levels were measured. A fasting muscle biopsy was obtained from the vastus lateralis for IR concentration and autophosphorylation activity measurements. These procedures were repeated 1 y after surgery.
  
  
  RESULTS
  At 1 y after surgery, the subjects had lost an average of 48.3+/-5.6 kg (P<0.001), insulin sensitivity had significantly increased as determined by the minimal model (SI 0.72+/-0.18 vs 3.86+/-1.43, P<0.05), and IR content had increased two-fold in muscle (2.1+/-0.4 vs 4.3+/-0.7 ng/mg protein, P<0.01). The increase in IR content was related to fasting insulin levels. In the subjects with the lowest IR function, there was also an increase in IR function. Plasma adiponectin increased by 40% following weight loss (7.4+/-1.6 pre vs 10.3+/-1.3 mg/ml post, P<0.05). There was no significant change in muscle content of the IR inhibitor, PC-1.
  
  
  CONCLUSIONS
  Increased IR content, most likely regulated by insulin levels, may be one contributor to the increased insulin sensitivity that occurs when morbidly obese patients undergo bariatric surgery.
authors.affiliation: Department of Medicine, Division of Diabetes and Endocrine Research, Mount Zion Medical Center, University of California, San Francisco, San Francisco, CA, USA.
authors.forename: C
authors.initials: C
authors.lastname: Pender
authors.forename: I D
authors.initials: ID
authors.lastname: Goldfine
authors.forename: C J
authors.initials: CJ
authors.lastname: Tanner
authors.forename: W J
authors.initials: WJ
authors.lastname: Pories
authors.forename: K G
authors.initials: KG
authors.lastname: MacDonald
authors.forename: P J
authors.initials: PJ
authors.lastname: Havel
authors.forename: J A
authors.initials: JA
authors.lastname: Houmard
authors.forename: J F
authors.initials: JF
authors.lastname: Youngren
mesh_terms: D052242:Adiponectin; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D015390:Gastric Bypass; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D009767:Obesity, Morbid / Q000150:complications / Q000378:metabolism* / Q000601:surgery; D011184:Postoperative Period; D011506:Proteins / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism*; D015431:Weight Loss
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins; D011972:Receptor, Insulin