ECE2010 Poster Presentations Diabetes (103 abstracts)
Chitotriosidase activity predicts endothelial dysfunction in type 2 diabetes mellitus
Cem Haymana 1 , Alper Sonmez 2 , Serkan Tapan 3 , Umut Safer 1 , Gürkan Celebi 1 , Ozlem Ozturk 3 , Halil Genc 1 , Teoman Dogru 5 , Ilker Tasci 1 , Gokhan Erdem 1 , Abdullah Taslipinar 2 , Aydogan Aydogdu 2 , Mahmut I Yilmaz 4 , Ismail Kurt 3 & Mustafa Kutlu 2
1Internal Medicine, Gulhane School of Medicine, Ankara, Turkey; 2Endocrinology, Gulhane School of Medicine, Ankara, Turkey; 3Biochemistry, Gulhane School of Medicine, Ankara, Turkey; 4Nephrology, Gulhane School of Medicine, Ankara, Turkey; 5Gastroenterology, Gulhane School of Medicine, Ankara, Turkey.
The enzyme chitotriosidase (ChT) is secreted by activated macrophages and play active role in human immune response. ChT activity is increased in atherosclerosis in association to the extent of the disease. We investigated the relevance of ChT to endothelial functions and insulin resistance in patients with T2DM.
Forty newly diagnosed and untreated patients with T2DM (male 17; age: 47.0±6.2 years) and 50 healthy volunteers (male 21; age: 50.2±8.8 years) were enrolled. Plasma asymmetric dimethyl arginine (ADMA) levels were determined by ELISA. ChT activity was measured by the fluorescence method. Insulin resistance was calculated by the HOMA-IR formula.
The patients had higher systolic blood pressures, HOMA-IR, ADMA levels and ChT activities (P<0.001 for all) and lower HDL cholesterol levels (P=0.03) than the control group. The ChT activities of the total group were significantly correlated to the age (r=0.031, P=0.003), ADMA (r=0.22, P=0.04) and plasma glucose levels (r=0.27, P=0.01). ChT was the independent determinant of the plasma ADMA levels (r=0.26, P=0.02).
The results of the present study show that serum ChT activity is increased in patients with newly diagnosed, untreated and uncomplicated patients with T2DM. The results also imply that increased ChT activity may be a predictor of endothelial dysfunction.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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