title: Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta.
abstract: OBJECTIVE
  Several epidemiological data suggest that patients with postprandial hyperglycaemia are at high risk of cardiovascular disease. The aim of this study was to elucidate the effect of a glucose 'spike' on monocyte adhesion to rat aortic endothelial cells.
  
  
  METHODS
  Monocyte adhesion to endothelial cells in vivo was quantitated using an en face method for observation of endothelial surface after immunohistochemical staining for CD68 in the thoracic aortas of Sprague-Dawley rats after several kinds of blood glucose rises.
  
  
  RESULTS
  The number of monocytes adhering to endothelial cells increased at 30 min after injection of glucose in 8-week-old Sprague-Dawley rats. The increased adhesion returned to the basal level at 120 min after glucose injection, concomitantly with the return of blood glucose levels to normal. The infusion of octreotide to inhibit endogenous insulin secretion did not prevent the glucose-induced increase in monocyte adhesion to endothelial cells. On the other hand, the number of monocytes adhering to endothelial cells did not increase in rats with streptozotocin-induced diabetes and sustained hyperglycaemia.
  
  
  CONCLUSIONS
  Our data demonstrate that a temporary rise in blood glucose levels can in itself promote a reversible increase in monocyte adhesion to arterial endothelial cells.
authors.affiliation: Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, 113-8421, Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Otsuka
authors.forename: K
authors.initials: K
authors.lastname: Azuma
authors.forename: T
authors.initials: T
authors.lastname: Iesaki
authors.forename: F
authors.initials: F
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Hirose
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: Y
authors.initials: Y
authors.lastname: Tanaka
authors.forename: H
authors.initials: H
authors.lastname: Daida
authors.forename: R
authors.initials: R
authors.lastname: Kawamori
authors.forename: H
authors.initials: H
authors.lastname: Watada
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001013:Aorta, Thoracic / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology; D001786:Blood Glucose / Q000032:analysis; D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects; D002452:Cell Count; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology*; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology; D006943:Hyperglycemia / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D007328:Insulin / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology; D008297:Male; D009000:Monocytes / Q000473:pathology / Q000502:physiology*; D015282:Octreotide / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001786:Blood Glucose; D005947:Glucose; D007328:Insulin; D015282:Octreotide; C067980:CD68 antigen, human; D000097382:CD68 Molecule