The glucose-dependent insulinotropic polypeptide and glucose-stimulated insulin response to exercise training and diet in obesity

Karen R Kelly, Latina M Brooks, Thomas P J Solomon, Sangeeta R Kashyap, Valerie B O'Leary, John P Kirwan

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)

Abstract

Aging and obesity are characterized by decreased beta-cell sensitivity and defects in the potentiation of nutrient-stimulated insulin secretion by GIP. Exercise and diet are known to improve glucose metabolism and the pancreatic insulin response to glucose, and this effect may be mediated through the incretin effect of GIP. The purpose of this study was to assess the effects of a 12-wk exercise training intervention (5 days/wk, 60 min/day, 75% Vo(2 max)) combined with a eucaloric (EX, n = 10) or hypocaloric (EX-HYPO, pre: 1,945 +/- 190, post: 1,269 +/- 70, kcal/day; n = 9) diet on the GIP response to glucose in older (66.8 +/- 1.5 yr), obese (34.4 +/- 1.7 kg/m(2)) adults with impaired glucose tolerance. In addition to GIP, plasma PYY(3-36), insulin, and glucose responses were measured during a 3-h, 75-g oral glucose tolerance test. Both interventions led to a significant improvement in Vo(2 max) (P < 0.05). Weight loss (kg) was significant in both groups but was greater after EX-HYPO (-8.3 +/- 1.1 vs. -2.8 +/- 0.5, P = 0.002). The glucose-stimulated insulin response was reduced after EX-HYPO (P = 0.02), as was the glucose-stimulated GIP response (P < 0.05). Furthermore, after the intervention, changes in insulin (DeltaI(0-30)/DeltaG(0-30)) and GIP (Delta(0-30)) secretion were correlated (r = 0.69, P = 0.05). The PYY(3-36) (Delta(0-30)) response to glucose was increased after both interventions (P < 0.05). We conclude that 1) a combination of caloric restriction and exercise reduces the GIP response to ingested glucose, 2) GIP may mediate the attenuated glucose-stimulated insulin response after exercise/diet interventions, and 3) the increased PYY(3-36) response represents an improved capacity to regulate satiety and potentially body weight in older, obese, insulin-resistant adults.

Original languageEnglish
Pages (from-to)E1269-74
JournalAmerican Journal of Physiology: Endocrinology and Metabolism
Volume296
Issue number6
DOIs
Publication statusPublished - Jun 2009

Keywords

  • Aged
  • Blood Glucose
  • Body Mass Index
  • Diet, Reducing
  • Eating
  • Exercise
  • Female
  • Gastric Inhibitory Polypeptide
  • Glucagon-Like Peptide 1
  • Humans
  • Insulin
  • Insulin Resistance
  • Male
  • Obesity
  • Peptide Fragments
  • Peptide YY
  • Physical Fitness
  • Satiety Response

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