title: Weight loss therapy improves pancreatic endocrine function in obese older adults.
abstract: OBJECTIVE
  Obesity and aging increase the risk of type 2 diabetes (T2D). We evaluated whether weight loss therapy improves pancreatic endocrine function and insulin sensitivity in obese older adults.
  
  
  METHODS
  Twenty-four obese (BMI: 38 +/- 2 kg/m(2)) older (age: 70 +/- 2 years) adults completed a 6-month randomized, controlled trial. Participants were randomized to diet and exercise (treatment group) or no therapy (control group). beta-Cell function (assessed using the C-peptide minimal model), alpha-cell function (assessed by the glucagon response to an oral glucose load), insulin sensitivity (assessed using the glucose minimal model), and insulin clearance rate were evaluated using a 5-h modified oral glucose tolerance test.
  
  
  RESULTS
  Body weight decreased in the treatment group, but did not change in the control group (-9 +/- 1% vs. 0 +/- 1%; P < 0.001). Insulin sensitivity doubled in the treatment group and did not change in the control group (116 +/- 49% vs. -11 +/- 13%; P < 0.05). Even though indices of beta-cell responsivity to glucose did not change (P > 0.05), the disposition index (DI), which adjusts beta-cell insulin response to changes in insulin sensitivity, improved in the treatment group compared with the control group (100 +/- 47% vs. -22 +/- 9%; P < 0.05). The glucagon response decreased in the treatment but not in the control group (-5 +/- 2% vs. 4 +/- 4%; P < 0.05). Insulin secretion rate did not change (P > 0.05), but insulin clearance rate increased (51 +/- 25%; P < 0.05), resulting in lower plasma insulin concentrations.
  
  
  CONCLUSIONS
  Weight loss therapy concomitantly improves beta-cell function, lowers plasma glucagon concentrations, and improves insulin action in obese older adults. These metabolic effects are likely to reduce the risk of developing T2D in this population.
authors.affiliation: Division of Geriatrics and Nutritional Science, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA. dvillare@wustl.edu
authors.forename: Dennis T
authors.initials: DT
authors.lastname: Villareal
authors.forename: Marian R
authors.initials: MR
authors.lastname: Banks
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Patterson
authors.forename: Kenneth S
authors.initials: KS
authors.lastname: Polonsky
authors.forename: Samuel
authors.initials: S
authors.lastname: Klein
mesh_terms: D000368:Aged; D000375:Aging / Q000502:physiology*; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D004038:Diet, Reducing; D015444:Exercise / Q000502:physiology*; D005260:Female; D005934:Glucagon / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D050417:Insulin-Secreting Cells / Q000502:physiology; D007515:Islets of Langerhans / Q000503:physiopathology*; D008297:Male; D009765:Obesity / Q000503:physiopathology*; D012307:Risk Factors; D015431:Weight Loss / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D007328:Insulin; D005934:Glucagon