title: Postload hyperglycemia is associated with increased subclinical inflammation in patients with prediabetes.
abstract: OBJECTIVE
  In this present study, we aimed: (i) To clarify if prediabetes is associated with subclinical inflammation independent of underlying obesity, and (ii) to evaluate the effect of postload glucose concentration on subclinical inflammation markers in a group of patients with elevated fasting glucose.
  
  
  METHODS
  In a cohort of 165 patients with newly detected fasting hyperglycemia, according to 75 g oral glucose tolerance test (OGTT), subjects were classified either as newly diagnosed type 2 diabetes (diabetes group, n = 40), impaired fasting glucose (IFG) plus impaired glucose tolerance (IGT) (IFG/IGT group, n = 42) or IFG only (IFG group, n = 83). A control group (n = 47) consisted of age- and body mass index (BMI)-matched healthy subjects with a normal OGTT. Circulating concentrations of lipids, insulin, interleukin-6 (IL-6), interleukin-8 (IL-8) and high sensitive C-reactive protein (hsCRP) were measured. HOMA index was calculated.
  
  
  RESULTS
  Subclinical inflammation markers were elevated in patients with diabetes and IFG/IGT compared to healthy controls and also IFG patients (diabetes vs. control: p < 0.05 for hsCRP, IL-8, and IL-6; IFG/IGT vs. control: p < 0.05 for hsCRP, and IL-6; diabetes vs. IFG: p < 0.05 for hsCRP, and IL-6; IFG/IGT vs. IFG: p < 0.05 for hsCRP, and IL-6). In multiple regression analysis, postload glucose concentration was independently associated with circulating hsCRP and IL-6 concentrations when the data was controlled for age, gender, BMI and lipid concentrations (p < 0.05 for hsCRP, and IL-6).
  
  
  CONCLUSIONS
  Our results suggest that patients with prediabetes, independent of underlying obesity, have increased concentrations of subclinical inflammation which is mostly driven by postload glucose concentrations.
authors.affiliation: Department of Clinical Biochemistry, Tepecik Training and Research Hospital, Izmir, Turkey. ayfercolak@gmail.com
authors.forename: Ayfer
authors.initials: A
authors.lastname: Colak
authors.forename: Baris
authors.initials: B
authors.lastname: Akinci
authors.forename: Gulden
authors.initials: G
authors.lastname: Diniz
authors.forename: Hakan
authors.initials: H
authors.lastname: Turkon
authors.forename: Faruk
authors.initials: F
authors.lastname: Ergonen
authors.forename: Hulya
authors.initials: H
authors.lastname: Yalcin
authors.forename: Isil
authors.initials: I
authors.lastname: Coker
mesh_terms: D000328:Adult; D058070:Asymptomatic Diseases; D001786:Blood Glucose; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000276:immunology; D005260:Female; D018149:Glucose Intolerance / Q000097:blood* / Q000276:immunology; D005951:Glucose Tolerance Test; D006801:Humans; D007249:Inflammation / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000276:immunology; D011236:Prediabetic State / Q000097:blood* / Q000276:immunology
chemical_list: D001786:Blood Glucose; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D002097:C-Reactive Protein