title: Insulin and non-insulin mediated vasodilation and glucose uptake in patients with type 2 diabetes.
abstract: OBJECTIVE
  The objective was to re-examine endothelial function, insulin mediated vasodilation and glucose extraction in the forearm of patients with type 2 diabetes (T2DM) and matched control subjects (CON) to investigate whether blood flow impairments result from diabetes per se or from concurrent disease.
  
  
  METHODS
  18 subjects (10 with T2DM, 8 CON) had graded brachial artery infusions of endothelial dependent (acetylcholine: 15, 30, 60 microg/min), endothelial independent (sodium nitroprusside: 1, 3, 10 microg/min) and partially endothelial mediated (adenosine: 50, 150, 500 microg/min) vasodilators. The protocol was repeated during a hyperinsulinemic clamp. Forearm blood flow and glucose extraction were measured at each dose of vasodilator (with/without insulin). Measurements were also taken in the control arm, reflecting systemic insulin infusion only.
  
  
  RESULTS
  Non-insulin mediated increases in bulk forearm blood flow were similar in T2DM and CON. However, insulin mediated forearm blood flow responses and glucose extraction were lower in T2DM versus CON.
  
  
  CONCLUSIONS
  The vasodilatory effect of insulin is impaired in T2DM although bulk flow capacity is maintained. Insulin mediated glucose extraction is reduced during concomitant maximal stimulation of forearm blood flow with endothelial-dependent vasodilators, despite maintaining flow. This is consistent with previous work that associates T2DM with impaired insulin mediated capillary recruitment.
authors.affiliation: Centre for Healthy Aging, Department of Biomedical Sciences, Section of Systems Biology Research, Faculty of Health Sciences, University of Copenhagen, Blegdamsvej 3, DK 2200 Copenhagen N, Denmark. celena@mfi.ku.dk
authors.forename: Celena
authors.initials: C
authors.lastname: Scheede-Bergdahl
authors.forename: David Benee
authors.initials: DB
authors.lastname: Olsen
authors.forename: Danny
authors.initials: D
authors.lastname: Reving
authors.forename: Robert
authors.initials: R
authors.lastname: Boushel
authors.forename: Flemming
authors.initials: F
authors.lastname: Dela
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage / Q000494:pharmacology; D000241:Adenosine / Q000008:administration & dosage / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D001794:Blood Pressure; D001916:Brachial Artery / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006207:Half-Life; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007261:Infusions, Intra-Arterial; D007328:Insulin / Q000494:pharmacology*; D008875:Middle Aged; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D010101:Oxygen Consumption; D012016:Reference Values; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D014665:Vasodilator Agents; D009599:Nitroprusside; D000241:Adenosine; D000109:Acetylcholine