التفاصيل البيبلوغرافية
| العنوان: |
A STUDY OF ANGIOTENSIN CONVERTING ENZYME GENE POLYMORPHISM IN THE PATIENTS WITH DIABETIC NEUROPATHY. |
| المؤلفون: |
Stoian, Adina, Bănescu, Claudia, Stoian, M., Buicu, Gabriela, Andreea, Chiotoroiu, Onişor, Danusia |
| المصدر: |
Acta Medica Transilvanica; sep2012, Vol. 17 Issue 3, p218-220, 3p |
| مصطلحات موضوعية: |
DIABETIC neuropathies, GENETIC polymorphisms, ANGIOTENSIN converting enzyme, PROTEIN kinase C, OXIDATIVE stress, PEOPLE with diabetes |
| Abstract (English): |
Neuropathies are a common complication of diabetes mellitus. There are a few theories to explain diabetic neuropathy: the polyol pathway theory, the oxidative stress, protein kinase C activation, and the glycosylation end-product theory; all contributes to microvascular injury involving small blood vessels that supply nerves and nerve dysfunction. It has become obvious that several pathophysiological factors probably operate simultaneously and it may be too simplistic to try to explain the many clinical presentations and pathological findings of diabetic neuropathy by a single theory. A lot of studies suggest that diabetic neuropathy may involve genetic susceptibility. The aim of this study was to investigate the influence of angiotensin-converting enzyme (ACE) gene I (insertion)/D (deletion) polymorphism in the development of diabetic neuropathy. The study consists of 23 patients with diabetic neuropathy and 20 without diabetic neuropathy. ACE polymorphism was detected by the restriction fragment length polymorphism method after a polymerase chain reaction. A significantly higher frequency of ACE I allele was observed in the diabetic neuropathy patients compared with the healthy control group where there was a higher frequency of ACE D allele. The distribution of ACE genotypes and alleles frequency showed differences between the patients with diabetic neuropathy and without this complication (p<0.05). Our results indicate that ACE D allele protects against diabetic neuropathy. [ABSTRACT FROM AUTHOR] |
| Abstract (Romanian): |
Neuropatiile sunt o complicaşie obiţnuită a diabetului zaharat. Există o serie de teorii care explică aparişia neuropatiei diabetice: calea poliol, stresul oxidativ, activarea proteinei C ţi teorii glicozilării proteinelor; toate acestea determină leziuni microvasculare care afectează vasele mici de sânge care irigă nervii periferici ţi determină în final disfuncşia acestora. Este evident că există o serie de factori care operează, probabil, simultan ţi ar părea prea simplist să încercăm să explicăm multiplele variante clinice de prezentare ţi modificările fiziopatologice din neuropatia diabetică prin intermediul unei simple teorii. O serie de studii sugerează că neuropatia diabetică poate să apară ţi ca urmare a unei susceptibilităşi genetice. Scopul acestui studiu este investigarea influenşei polimorfismului I (inserşie)/D (deleşie) al genei enzimei de conversie a angiotensinei în dezvoltarea neuropatiei diabetice. Studiul a inclus 86 de pacienşi cu neuropatie diabetică ţi 90 de pacienşi fără neuropatie diabetică. Pentru analiza polimorfismului ACE I/D s-a folosit reacţia polimerizării în lanţ şi polimorfismul fragmentelor de restricţie. S-a observat o frecvenşă semnificativ mai mare a alelei D a ACE la pacienşii cu neuropatie diabetică comparativ cu grupul de control format din pacienşi sănătoţi unde s-a observat o frecvenşă mai mare a alelei I. Distribuşia genotipului ACE ţi frecvenşa alelelor a arătat diferenşe între grupul pacienşilor cu neuropatie diabetică ţi grupul de control (p<0.05). Rezultatele noastre indică faptul că alela I protejează împotriva neuropatiei diabetice. [ABSTRACT FROM AUTHOR] |
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