title: A low-glycemic index diet combined with exercise reduces insulin resistance, postprandial hyperinsulinemia, and glucose-dependent insulinotropic polypeptide responses in obese, prediabetic humans.
abstract: BACKGROUND
  The optimal lifestyle intervention that reverses diabetes risk factors is not known.
  
  
  OBJECTIVE
  We examined the effect of a low-glycemic index (GI) diet and exercise intervention on glucose metabolism and insulin secretion in obese, prediabetic individuals.
  
  
  METHODS
  Twenty-two participants [mean ± SEM age: 66 ± 1 y; body mass index (in kg/m(2)): 34.4 ± 0.8] underwent a 12-wk exercise-training intervention (1 h/d for 5 d/wk at ≈ 85% of maximum heart rate) while randomly assigned to receive either a low-GI diet (LoGIX; 40 ± 0.3 units) or a high-GI diet (HiGIX; 80 ± 0.6 units). Body composition (measured by using dual-energy X-ray absorptiometry and computed tomography), insulin sensitivity (measured with a hyperinsulinemic euglycemic clamp with [6,6-(2)H(2)]-glucose), and oral glucose-induced insulin and incretin hormone secretion were examined.
  
  
  RESULTS
  Both groups lost equal amounts of body weight (-8.8 ± 0.9%) and adiposity and showed similar improvements in peripheral tissue (+76.2 ± 14.9%) and hepatic insulin sensitivity (+27.1 ± 7.1%) (all P < 0.05). However, oral glucose-induced insulin secretion was reduced only in the LoGIX group (6.59 ± 0.86 nmol in the prestudy compared with 4.70 ± 0.67 nmol in the poststudy, P < 0.05), which was a change related to the suppressed postprandial response of glucose-dependent insulinotropic polypeptide. When corrected for changes in β cell glucose exposure, changes in insulin secretion were attenuated in the LoGIX group but became significantly elevated in the HiGIX group.
  
  
  CONCLUSIONS
  Although lifestyle-induced weight loss improves insulin resistance in prediabetic individuals, postprandial hyperinsulinemia is reduced only when a low-GI diet is consumed. In contrast, a high-GI diet impairs pancreatic β cell and intestinal K cell function despite significant weight loss. These findings highlight the important role of the gut in mediating the effects of a low-GI diet on type 2 diabetes risk reduction.
authors.affiliation: Department of Pathobiology, Lerner Research Institute and Nutrition, Case Western Reserve University, Cleveland, OH, USA. kirwanj@ccf.org
authors.forename: Thomas Pj
authors.initials: TP
authors.lastname: Solomon
authors.forename: Jacob M
authors.initials: JM
authors.lastname: Haus
authors.forename: Karen R
authors.initials: KR
authors.lastname: Kelly
authors.forename: Marc D
authors.initials: MD
authors.lastname: Cook
authors.forename: Julianne
authors.initials: J
authors.lastname: Filion
authors.forename: Michael
authors.initials: M
authors.lastname: Rocco
authors.forename: Sangeeta R
authors.initials: SR
authors.lastname: Kashyap
authors.forename: Richard M
authors.initials: RM
authors.lastname: Watanabe
authors.forename: Hope
authors.initials: H
authors.lastname: Barkoukis
authors.forename: John P
authors.initials: JP
authors.lastname: Kirwan
mesh_terms: D050154:Adiposity / Q000502:physiology; D000368:Aged; D003131:Combined Modality Therapy; D015444:Exercise / Q000502:physiology*; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005951:Glucose Tolerance Test; D038321:Glycemic Index; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000628:therapy*; D007328:Insulin / Q000097:blood* / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D008099:Liver / Q000503:physiopathology; D008297:Male; D009765:Obesity / Q000097:blood / Q000178:diet therapy / Q000628:therapy*; D019518:Postprandial Period; D015431:Weight Loss / Q000502:physiology*
chemical_list: D007328:Insulin; D005749:Gastric Inhibitory Polypeptide