Naslov
Intestinal activity of dipeptidyl peptidase IV(DPPIV, CD 26)in patients with coeliac disease
(Intestinal activity of dipeptidyl peptidase IV(DPPIV/CD 26)in patients with coeliac disease)

Autori
Varljen, Jadranka ; Detel, Dijana ; Pavletić, Martina ; Frleta, Neven ; Peršić, Mladen

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
ESF Programme in Functional Genomic:1st Conference / - Prag, 2003, 138-138

Skup
ESF Functional Genomic and disease: 1st Conference

Mjesto i datum
Prag, Češka Republika, 14.05.2003. - 17.05.2003

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Intestinal activity; dipeptidyl peptidase IV; coeliac disease

Sažetak
CD26 is a multifunctional type II cell surface transmembrane glycoprotein widely expressed on epithelial end endothelial cells of various organs including the liver, kidneys and the gastrointestinal tract. CD26 possesses a known dipeptidyl-peptidase activity(DPPIV) in its extracellular domain, which cleaves X-proline dipeptides from the N-terminus of polypeptides. Coeliac disease(CD) is a human, genetically linked disorder that develops in gluten-sensitive people. The mechanism responsible for the small intestinal damage characteristic of CD is still unknown. However, it has been found that the expression of CD26 is decreased on the surface of epithelial cells of the small intestine in patients with CD. The relationship between symptoms, intestinal mucosal histology and DPPIV activity is not well defined. Therefore, we decided to test the hypothesis that the activity of DPPIV is lowered in patients with CD. DPPIV activity and the histology of endoscopically obtained small intestinal biopsies were followed during a 2-year period in patients with malabsorption syndrome(n=80). On the basis of histological findings and endomisium antibodies we divided our patients in two groups: in the first group malabsorption was caused by the CD, whereas in the second group it was caused by other factors. Histological changes within groups were classified based on the grade of mucosal villous atrophy. The intestinal DPPIV activity was decreased in both groups and showed an inverse correlation with small intestinal damage. According to the grade of mucosal villous atrophy, DPPIV activity was significantly more decreased in the group of patients with CD than in the other group of patients with the same degree of histological damage(p<0.05). In the future, we are planing to induce CD in CD26+/+ and CD26-/- mice in order to determine the relationship between CD26 and the disease, and the possible molecular mechanisms by which this molecule contributes to malnutrition in coeliac disease.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA