title: Effects of transoral gastroplasty on glucose homeostasis in obese subjects.
abstract: OBJECTIVE
  Transoral gastroplasty (TOGA) is a safe and less invasive procedure than traditional bariatric surgery. We studied the effects of TOGA on the risk of progression from prediabetes to overt type 2 diabetes mellitus (T2DM) or on regression from diabetes or prediabetes to a lower risk category.
  
  
  METHODS
  Prospective, observational study (October 2008 to October 2010) performed at Catholic University, Rome, Italy. Fifty consecutive subjects 18-60 years old, 35 ≥ body mass index < 55 kg/m², were enrolled. Glucose tolerance, insulin sensitivity, and secretion were studied at baseline and 1 week and 1, 6, and 12 months after TOGA. Plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), and ghrelin levels were measured.
  
  
  RESULTS
  Forty-three patients (86%) completed the 1-year postoperative follow-up. Patients lost 16.90% of baseline weight (P level × factor time <0.001). Body mass index decreased from 42.24 ± 3.43 to 34.65 ± 4.58 kg/m² (P < .001). Twenty-three patients (53.5%) were diagnosed as normal glucose tolerance (NGT) before treatment, 2 (4.6%) were impaired fasting glucose (IFG), 12 (27.9%) were impaired glucose tolerance (IGT), 1 (2.3%) had both IFG and IGT, and 5 (11.6%) had T2DM. At 1-year posttreatment, the percentages changed to 86.0% NGT, 2.3% IFG, 11.6% IGT, 0% IFG plus IGT, and 0% T2DM, respectively. Peripheral insulin resistance and homeostasis model of assessment-insulin resistance improved significantly. Fasting glucose-dependent insulinotropic peptide and ghrelin decreased from 316.9 ± 143.1 to 156.2 ± 68.2 pg/mL (P < .001) and from 630.6 ± 52.1 to 456.7 ± 73.1 pg/mL (P < .001), respectively, whereas GLP-1 increased from 16.2 ± 4.9 to 23.7 ± 9.5 pg/mL (P < .001).
  
  
  CONCLUSIONS
  TOGA induced glucose disposal improvement with regression of diabetes to NGT or IGT and regression of IGT and IFG to NGT in half of the cases. Regressors showed a much larger increase of GLP-1 levels than progressors.
authors.affiliation: Department of Internal Medicine, Catholic University, Rome, Italy.
authors.forename: Laura
authors.initials: L
authors.lastname: Leccesi
authors.forename: Simona
authors.initials: S
authors.lastname: Panunzi
authors.forename: Andrea
authors.initials: A
authors.lastname: De Gaetano
authors.forename: Pietro
authors.initials: P
authors.lastname: Familiari
authors.forename: Amerigo
authors.initials: A
authors.lastname: Iaconelli
authors.forename: Caterina
authors.initials: C
authors.lastname: Guidone
authors.forename: Ada
authors.initials: A
authors.lastname: Mazzarella
authors.forename: Guido
authors.initials: G
authors.lastname: Costamagna
authors.forename: Geltrude
authors.initials: G
authors.lastname: Mingrone
mesh_terms: D000293:Adolescent; D000328:Adult; D015992:Body Mass Index; D003327:Coronary Disease / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D018450:Disease Progression; D005500:Follow-Up Studies; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D015391:Gastroplasty; D054439:Ghrelin / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D006801:Humans; D007333:Insulin Resistance; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D009767:Obesity, Morbid / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D011236:Prediabetic State / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology*; D011446:Prospective Studies; D012306:Risk; D012384:Rome / Q000453:epidemiology; D015431:Weight Loss; D055815:Young Adult
chemical_list: C515349:GHRL protein, human; D054439:Ghrelin; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1