title: Occult impaired glucose regulation in patients with atherosclerosis is associated to the number of affected vascular districts and inflammation.
abstract: OBJECTIVE
  The role of inflammatory adipokines has clear mechanistic effects in the promotion of both DM2 and cardiovascular diseases (CVDs), but it is unknown to what extent atherosclerosis-related inflammation might promote defects of glucose metabolism. The purpose of this study was to test the hypothesis that in subjects with atherosclerotic vascular disease and no previous medical record of type 2 diabetes mellitus (DM2), the diagnosis of occult impaired glucose regulation (IGR) is related to the severity of atherosclerosis, measured as the single or combined presence of an history of coronary artery disease (CAD), carotid atherosclerosis (Car-ATS) and peripheral artery disease (PAD).
  
  
  METHODS
  In a population of 551 subjects (440 men and 111 women) with a previous history of atherosclerosis, we investigated the presence of IGR (including both impaired glucose tolerance and DM2). To test the correlation between conventional and non-conventional risk factors for cardiovascular disease and diabetes we used logistic and regression analysis models.
  
  
  RESULTS
  IGR was more prevalent in patients with a documented vascular disease in two or three vessel districts compared with patients with only one symptomatic district (p=0.016). Among classic risk factors we found that waist circumference was correlated neither to IGR nor to symptomatic vascular disease extension. By contrast, adiponectin level was independently associated to vascular and glucose regulation status (p=0.012 and p<0.001, respectively).
  
  
  CONCLUSIONS
  In subjects affected by atherosclerotic vascular diseases, the presence of impaired glucose regulation is associated to the number of vascular districts affected and to a reduced adiponectin level.
authors.affiliation: Department of Internal Medicine, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy.
authors.forename: Stefano
authors.initials: S
authors.lastname: Rizza
authors.forename: Marina
authors.initials: M
authors.lastname: Cardellini
authors.forename: Eugenio
authors.initials: E
authors.lastname: Martelli
authors.forename: Ottavia
authors.initials: O
authors.lastname: Porzio
authors.forename: Chiara
authors.initials: C
authors.lastname: Pecchioli
authors.forename: Antonio
authors.initials: A
authors.lastname: Nicolucci
authors.forename: Nikolaus
authors.initials: N
authors.lastname: Marx
authors.forename: Davide
authors.initials: D
authors.lastname: Lauro
authors.forename: Arnaldo
authors.initials: A
authors.lastname: Ippoliti
authors.forename: Franco
authors.initials: F
authors.lastname: Romeo
authors.forename: Renato
authors.initials: R
authors.lastname: Lauro
authors.forename: Massimo
authors.initials: M
authors.lastname: Federici
mesh_terms: D052242:Adiponectin / Q000097:blood; D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000453:epidemiology*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000453:epidemiology; D016009:Chi-Square Distribution; D003324:Coronary Artery Disease / Q000453:epidemiology; D003430:Cross-Sectional Studies; D015536:Down-Regulation; D005260:Female; D018149:Glucose Intolerance / Q000097:blood / Q000453:epidemiology*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000453:epidemiology*; D018836:Inflammation Mediators / Q000097:blood; D007558:Italy / Q000453:epidemiology; D016014:Linear Models; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000453:epidemiology; D015995:Prevalence; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D055105:Waist Circumference
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D018836:Inflammation Mediators