PMID- 11758971 OWN - NLM STAT- MEDLINE DCOM- 20020107 LR - 20221207 IS - 1078-0297 (Print) IS - 1078-0297 (Linking) VI - 108 IP - 1-2 DP - 2000 Jul-Aug TI - Progression of carotid atherosclerosis and the role of endothelin in diabetic patients. PG - 27-37 AB - 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. FAU - Migdalis, I N AU - Migdalis IN AD - Department of Diabetes, NIMTS Hospital, Athens, Greece. FAU - Kalogeropoulou, K AU - Kalogeropoulou K FAU - Iiopoulou, V AU - Iiopoulou V FAU - Varvarigos, N AU - Varvarigos N FAU - Karmaniolas, K D AU - Karmaniolas KD FAU - Mortzos, G AU - Mortzos G FAU - Cordopatis, P AU - Cordopatis P LA - eng PT - Clinical Trial PT - Journal Article PL - United States TA - Res Commun Mol Pathol Pharmacol JT - Research communications in molecular pathology and pharmacology JID - 9437512 RN - 0 (Blood Glucose) RN - 0 (Endothelins) RN - 0 (Glycated Hemoglobin A) RN - 0 (Insulin) RN - 0 (Lipid Peroxides) RN - 0 (Thiobarbituric Acid Reactive Substances) RN - 58962-34-8 (6-Ketoprostaglandin F1 alpha) SB - IM MH - 6-Ketoprostaglandin F1 alpha/blood MH - Arteriosclerosis/*pathology MH - Blood Glucose/metabolism MH - Body Mass Index MH - Carotid Arteries/pathology MH - Carotid Artery Diseases/*pathology MH - Diabetes Mellitus, Type 2/*pathology MH - Disease Progression MH - Endothelins/*physiology MH - Female MH - Glycated Hemoglobin/metabolism MH - Humans MH - Insulin/blood MH - Lipid Peroxides/physiology MH - Male MH - Middle Aged MH - Thiobarbituric Acid Reactive Substances/metabolism EDAT- 2002/01/05 10:00 MHDA- 2002/01/10 10:01 CRDT- 2002/01/05 10:00 PHST- 2002/01/05 10:00 [pubmed] PHST- 2002/01/10 10:01 [medline] PHST- 2002/01/05 10:00 [entrez] PST - ppublish SO - Res Commun Mol Pathol Pharmacol. 2000 Jul-Aug;108(1-2):27-37.