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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Mangiafico R. A., Malatino L. S., Santonocito M., Spada R. S.
From the Institute of Internal Medicine “L. Condorelli”, University of Catania, Catania, Italy
Background. Endothelin-1 (ET-1), a vasoconstrictor and mitogenic endothelium-derived peptide, has been considered as a marker for endothelial damage and potential contributor to the development of the atherogenic process.
Methods. To evaluate the pattern of plasma ET-1 secretion in non-insulin-dependent diabetes mellitus (NIDDM) and nondiabetic patients with chronic arterial obstructive disease (CAOD) of the lower limbs, plasma levels of ET-1 were determined in 12 NIDDM patients (10 men and 2 women; mean age 63±8 years) with CAOD of the lower limbs at Fontaine stage II and in 12 nondiabetic patients (11 men and 1 woman; mean age 62±4 years) with comparable arteriopathy. Ten normal subjects comprised the control population.
Results. The plasma levels of ET-1 in NIDDM patients with CAOD of the lower limbs were 5.7±0.3 pmol/L, which represented a significant (p<0.001) difference from the values in nondiabetic patients with comparable arteriopathy (4.1±0.6 pmol/L) and those in the control group (2.7±0.7 pmol/L). Plasma levels of ET-1 showed a significant (p<0.0001) positive correlation with the levels of fasting insulin in NIDDM patients with CAOD of the lower limbs. Increased plasma ET-1 could reflect a major and/or more diffuse endothelial cell damage or dysfunction in NIDDM than in nondiabetic patients with comparable CAOD of the lower limbs. Augmented mitogenic ET-1 levels could also have a role both in diabetic and nondiabetic angiopathy.
Conclusions. The positive correlation between ET-1 plasma levels and fasting insulin levels in NIDDM patients with CAOD of the lower limbs suggests that the increased ET-1 release could be related to the augmented insulin secretion in these patients. Insulin-related overproduction of ET-1 could promote the atherogenic process and enhance the vascular tone to a greater extent in NIDDM than in nondiabetic patients with CAOD of the lower limbs.