title: Insulin resistance may contribute to vascular dysfunction in patients with chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Patients with chronic obstructive pulmonary disease (COPD) are at an increased cardiovascular risk; however, the underlying mechanisms for this relationship are ill defined. Altered glucose metabolism may increase cardiovascular risk via impaired endothelial function.
  
  
  METHODS
  We conducted a longitudinal pilot study to assess the interrelationship between systemic vascular function, glucose metabolism, and lung function in patients with COPD. Eighteen non-smoking patients with stable moderate-to-severe COPD [67 % male; median (first to third quartiles) Forced Expiratory Volume in 1 second (FEV1) % predicted: 38 % (28-55 %); body mass index: 26 kg/m(2) (24-28 kg/m(2))] free from cardiovascular risk factors were evaluated. Systemic vascular function was assessed by means of flow-mediated dilation technique of the brachial artery. Laboratory measurements included fasting blood glucose levels, circulating concentrations of insulin, C-reactive protein, and fibrinogen. Homeostatic model assessment of insulin resistance (HOMA-IR) was determined. Measurements were performed at baseline and were repeated after 12 months.
  
  
  RESULTS
  Flow-mediated dilation significantly decreased from 13.5 % (11-15 %) at baseline to 9.8 % (6-12 %; p = 0.002) at the follow-up visit, whereas both fasting blood glucose concentrations and HOMA-IR increased from 94 mg/dl (86-103 mg/dl) to 102 mg/dl (94-111 mg/dl; p = 0.027) and from 1.2 (0.8-2.1) to 1.7 (1.2-3.0; p = 0.023), respectively. There was a significant relationship between changes in endothelial function and changes in fasting serum glucose (r = - 0.483, p = 0.009), HOMA-IR (r = - 0.441, p = 0.019), and FEV1 (r = 0.336, p = 0.05).
  
  
  CONCLUSIONS
  Altered glucose metabolism may be associated with progression of endothelial dysfunction in patients with COPD.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Ludwig Boltzmann Institute for COPD, Otto Wagner Hospital, Sanatoriumstrasse 2, 1140, Vienna, Austria.
authors.forename: Matthias Helmut
authors.initials: MH
authors.lastname: Urban
authors.forename: Leyla
authors.initials: L
authors.lastname: Ay
authors.forename: Georg-Christian
authors.initials: GC
authors.lastname: Funk
authors.forename: Otto Chris
authors.initials: OC
authors.lastname: Burghuber
authors.forename: Philipp
authors.initials: P
authors.lastname: Eickhoff
authors.forename: Michael
authors.initials: M
authors.lastname: Wolzt
authors.forename: Arschang
authors.initials: A
authors.lastname: Valipour
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000503:physiopathology*; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000209:etiology / Q000503:physiopathology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000503:physiopathology*; D014664:Vasodilation
chemical_list: D001786:Blood Glucose; D007328:Insulin