title: Glucoregulatory physiology in subjects with low-normal, high-normal, or impaired fasting glucose.
abstract: OBJECTIVE
  We determined whether variations in fasting plasma glucose (FPG) within the nondiabetic range represent differences in insulin action or secretion.
  
  
  METHODS
  Using results of the 75-g oral glucose tolerance test, we classified 39 adults (body mass index range 20-56 kg/m2) as having normal fasting glucose (NFG, <100 mg/dl, n = 24) or impaired fasting glucose (IFG, 100-125 mg/dl, n = 15). The NFG group was subdivided into low-NFG (<90 mg/dl, n = 11) and high-NFG (90-99 mg/dl, n = 13). The 2-h oral glucose tolerance test plasma glucose value was used to assign normal or impaired glucose tolerance (IGT) status. Insulin sensitivity was assessed by hyperinsulinemic euglycemic clamp, quantitative insulin sensitivity check index, and homeostasis model assessment of insulin resistance; beta-cell function was assessed by calculating the insulinogenic index, homeostasis model assessment, and the disposition index.
  
  
  RESULTS
  Compared with low-NFG subjects, insulin sensitivity and glucose tolerance were lower among persons with isolated IFG and combined IFG-IGT. The hyperinsulinemic euglycemic clamp (micromol/kg x min(-1)/pmol/liter) was 0.109 +/- 0.011 in low-NFG subjects, 0.088 +/- 0.009 in IFG subjects (P = 0.04), and 0.022 +/- 0.003 in IFG-IGT subjects (P = 0.0014). The spread in FPG from 70-125 mg/dl was associated with a greater than 3-fold difference in insulin sensitivity. Compared with low-NFG subjects, the disposition index decreased by 32.8% in high-NFG subjects (P = 0.08), by 45.6% in subjects with isolated IFG (P < 0.02), and by 49.8% (P < 0.02) in those with combined IFG-IGT.
  
  
  CONCLUSIONS
  Compared with persons with low-NFG, those with IFG or combined IFG-IGT have significant alteration of glucoregulatory physiology, whereas high-NFG (pre-prediabetes) status might portend nascent glucoregulatory perturbations.
authors.affiliation: Division of Endocrinology, Diabetes, and Metabolism, University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, Tennessee 38163, USA. sdj@utmem.edu
authors.forename: Samuel
authors.initials: S
authors.lastname: Dagogo-Jack
authors.forename: Hasan
authors.initials: H
authors.lastname: Askari
authors.forename: Gunjan
authors.initials: G
authors.lastname: Tykodi
mesh_terms: D000328:Adult; D050260:Carbohydrate Metabolism / Q000502:physiology; D005215:Fasting / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D015309:Glucose Clamp Technique; D018149:Glucose Intolerance / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000502:physiology; D008297:Male
chemical_list: D007328:Insulin; D005947:Glucose