title: Progression of carotid atherosclerosis and the role of endothelin in diabetic patients.
abstract: An increased thickness of the carotid artery wall is thought to be a sign of early atherosclerosis. Since vascular endothelium is the site of formation of several substances, we have investigated the rate of progression of carotid atherosclerosis and the contribution of endothelin (ET-1), lipid peroxides [measured as thiobarbituric acid reacting species (TBARS)] and 6-keto-Prostaglandin-F1A (6-keto-PG-F1A) at baseline and after 30-months. Fifty patients with Type 2 diabetes without evidence of macroangiopathy, hypertension, proteinuria or proliferative retinopathy, and 27 healthy, non-diabetic persons were studied. Arterial wall thickness was measured as the mean of the maximum intimal-medial thickness (IMT) in 16 carotid segments by b-mode ultrasound. The IMT values was significantly increased in diabetic subjects (at baseline: 1110 +/- 310 microm, after 30 months: 1260 +/- 280 microm, p < 0.01), but not in control subjects (1100 +/- 280 microm, 1200 +/- 290 microm, respectively). At baseline time both groups had similar levels of ET-1, TBARS and 6-keto-PG-F1A. In 30-months follow-up, the ET-1 level 8.0 pmol/l (5.8-10.7) was significantly elevated in diabetic subjects, compared with the level at baseline time 7.43 pmol/l (4.8-11.1) p < 0.01. No significant differences were found in the other examined parameters in the studied groups. Although insulin levels remained unchanged in the two studied groups, in 30 months follow-up, the insulin level in the diabetic subjects, 92.4 +/- 35.1 pmol/l was significantly elevated compared with those of control subjects 76.0 +/- 31.0 pmol/l, p < 0.05. In conclusion, endothelis is the main associate of the change of IMT value over 30 months in diabetic patients, in whom the extent of atherosclerosis was significantly greater than in control subjects.
authors.affiliation: Department of Diabetes, NIMTS Hospital, Athens, Greece.
authors.forename: I N
authors.initials: IN
authors.lastname: Migdalis
authors.forename: K
authors.initials: K
authors.lastname: Kalogeropoulou
authors.forename: V
authors.initials: V
authors.lastname: Iiopoulou
authors.forename: N
authors.initials: N
authors.lastname: Varvarigos
authors.forename: K D
authors.initials: KD
authors.lastname: Karmaniolas
authors.forename: G
authors.initials: G
authors.lastname: Mortzos
authors.forename: P
authors.initials: P
authors.lastname: Cordopatis
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D001161:Arteriosclerosis / Q000473:pathology*; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002339:Carotid Arteries / Q000473:pathology; D002340:Carotid Artery Diseases / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology*; D018450:Disease Progression; D016232:Endothelins / Q000502:physiology*; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D008054:Lipid Peroxides / Q000502:physiology; D008297:Male; D008875:Middle Aged; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D015121:6-Ketoprostaglandin F1 alpha; D001786:Blood Glucose; D016232:Endothelins; D006442:Glycated Hemoglobin; D007328:Insulin; D008054:Lipid Peroxides; D017392:Thiobarbituric Acid Reactive Substances