Linked Life Data

15156690

Source:http://linkedlifedata.com/resource/pubmed/id/15156690

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2004-5-25
pubmed:abstractText
ACE gene insertion/deletion (I/D) polymorphism is a well-known risk factor of hypertension, cardiovascular diseases and progression of diabetic nephropathy. In carriers of allele D, serum level of angiotensin-II is higher, which can be associated with increased oxidative stress and subsequent endothelial damage. Albuminuria is a sensitive marker of endothelial damage, while serum activity of the enzyme gamma-glutamyl transferase--that plays important role in the antioxidant defense--may refer to the level of oxidative stress. The present paper reports on a cross-sectional clinical study, where authors have examined on the relation between ACE gene insertion/deletion polymorphism and carbohydrate metabolism, hypertension as well as albuminuria in type 2 diabetics (n = 145). In patients carrying allele D, fructosamine levels were significantly higher (p = 0.007) than in carriers of allele I. Patients with II + ID genotypes and those who were treated with insulin took more antihypertensive drugs than the ones with II genotype or orally treated (p = 0.015). They found a significant association between genotype and fructosamine level (p = 0.023). Association between genotype or modality of treatment of diabetes (oral vs, insulin) and combined treatment of hypertension (number of antihypertensive drugs) was of borderline significance. They found that fructosamin level of patients receiving ACE inhibitor was lower than that of patients not receiving ACE inhibitors. In patients with allele D, they have also found higher activity of gamma-GT and higher albuminuria. From this results and data of the literature the authors conclude that because of insulin resistance (in connection with the presence of allele D), these patients tend to have a worse metabolic state, more advanced glycation products, due to which oxidative stress and endothelial cell damage may develop. As albuminuria and activity of gamma-GT were both found higher in patients with allele D, and our patients did not suffer of any hepatic disease, authors take the consequence that gamma-GT is a marker of the oxidative stress caused by allele D. Endothelial damage may explain that these patients take a higher number of antihypertensive combination. Based on this, D allele may contribute--via increased glycation and oxidative stress--to the target organ damage in type 2 diabetes.
pubmed:language
hun
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0030-6002
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
855-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15156690-Adult, pubmed-meshheading:15156690-Aged, pubmed-meshheading:15156690-Aged, 80 and over, pubmed-meshheading:15156690-Antihypertensive Agents, pubmed-meshheading:15156690-Blood Glucose, pubmed-meshheading:15156690-Blood Pressure, pubmed-meshheading:15156690-Carbohydrate Metabolism, pubmed-meshheading:15156690-Cross-Sectional Studies, pubmed-meshheading:15156690-Diabetes Mellitus, Type 2, pubmed-meshheading:15156690-Female, pubmed-meshheading:15156690-Fructosamine, pubmed-meshheading:15156690-Gene Deletion, pubmed-meshheading:15156690-Humans, pubmed-meshheading:15156690-Hypertension, pubmed-meshheading:15156690-Hypertension, Renovascular, pubmed-meshheading:15156690-Hypoglycemic Agents, pubmed-meshheading:15156690-Insulin, pubmed-meshheading:15156690-Kidney Function Tests, pubmed-meshheading:15156690-Male, pubmed-meshheading:15156690-Middle Aged, pubmed-meshheading:15156690-Mutagenesis, Insertional, pubmed-meshheading:15156690-Oxidative Stress, pubmed-meshheading:15156690-Peptidyl-Dipeptidase A, pubmed-meshheading:15156690-Polymorphism, Genetic
pubmed:year
2004
pubmed:articleTitle
[Effect of ACE gene polymorphism on carbohydrate metabolism, on oxidative stress and on end-organ damage in type-2 diabetes mellitus].
pubmed:affiliation
Pécsi Tudományegyetem, Altalános Orvostudományi Kar, II. Belgyógyászati Klinika és Nephrologiai Centrum. gergo.molnar@aok.pte.hu
pubmed:publicationType
Journal Article, English Abstract