Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination

Genetic susceptibility plays an important role in the risk of developing chronic complications in patients with type 2 diabetes mellitus (T2DM). Aims. In this study, we evaluated the possible association of the polymorphic variants that encode key renal damage mediators (endothelial dysfunction, li...

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Autores principales: Anna Viktorovna Zheleznyakova, Nadezhda Olegovna Lebedeva, Olga Konstantinovna Vikulova, Valery Vyacheslavovich Nosikov, Minara Shamkhalovna Shamkhalova, Marina Vladimirovna Shestakova
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Publicado: Endocrinology Research Centre 2014
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spelling oai:doaj.org-article:237d2a0144b948ea8e9f69bc145928042021-11-14T09:00:19ZRisk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination2072-03512072-037810.14341/DM2014323-30https://doaj.org/article/237d2a0144b948ea8e9f69bc145928042014-10-01T00:00:00Zhttps://www.dia-endojournals.ru/jour/article/view/6693https://doaj.org/toc/2072-0351https://doaj.org/toc/2072-0378Genetic susceptibility plays an important role in the risk of developing chronic complications in patients with type 2 diabetes mellitus (T2DM). Aims. In this study, we evaluated the possible association of the polymorphic variants that encode key renal damage mediators (endothelial dysfunction, lipid metabolism and insulin secretion/sensitivity) with the risk of chronic kidney disease (CKD) in patients with T2DM. Materials and Methods. We enrolled 435 patients with T2DM using case-control study design. In 253 patients, we used non-overlapping criteria to form groups with/without CKD (defined as GFR=10 years) (n=75 and 178, respectively) and analysed the following 4 polymorphic markers: I/D in ACE, ecNOS4a/4b in NOS3, I/D in APOB and e2/e3/e4 in APOE genes. We then divided 182 patients in groups with/without CKD (n=38 and 144, respectively) regardless of the duration of diabetes and studied pro12ala in PPARG2, rs5219 in KCNJ11, rs12255372 in TCF7L2 and rs13266634 in SLC30A8 genes. 2 test, and data were expressed as odds ratios (ORs) with 95% confidence intervals (CIs). Values of pAnna Viktorovna ZheleznyakovaNadezhda Olegovna LebedevaOlga Konstantinovna VikulovaValery Vyacheslavovich NosikovMinara Shamkhalovna ShamkhalovaMarina Vladimirovna ShestakovaEndocrinology Research Centrearticlediabetes mellitusgenesckdnos3apobtcf7l2kcnj11Nutritional diseases. Deficiency diseasesRC620-627ENRUСахарный диабет, Vol 17, Iss 3, Pp 23-30 (2014)
institution DOAJ
collection DOAJ
language EN
RU
topic diabetes mellitus
genes
ckd
nos3
apob
tcf7l2
kcnj11
Nutritional diseases. Deficiency diseases
RC620-627
spellingShingle diabetes mellitus
genes
ckd
nos3
apob
tcf7l2
kcnj11
Nutritional diseases. Deficiency diseases
RC620-627
Anna Viktorovna Zheleznyakova
Nadezhda Olegovna Lebedeva
Olga Konstantinovna Vikulova
Valery Vyacheslavovich Nosikov
Minara Shamkhalovna Shamkhalova
Marina Vladimirovna Shestakova
Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination
description Genetic susceptibility plays an important role in the risk of developing chronic complications in patients with type 2 diabetes mellitus (T2DM). Aims. In this study, we evaluated the possible association of the polymorphic variants that encode key renal damage mediators (endothelial dysfunction, lipid metabolism and insulin secretion/sensitivity) with the risk of chronic kidney disease (CKD) in patients with T2DM. Materials and Methods. We enrolled 435 patients with T2DM using case-control study design. In 253 patients, we used non-overlapping criteria to form groups with/without CKD (defined as GFR=10 years) (n=75 and 178, respectively) and analysed the following 4 polymorphic markers: I/D in ACE, ecNOS4a/4b in NOS3, I/D in APOB and e2/e3/e4 in APOE genes. We then divided 182 patients in groups with/without CKD (n=38 and 144, respectively) regardless of the duration of diabetes and studied pro12ala in PPARG2, rs5219 in KCNJ11, rs12255372 in TCF7L2 and rs13266634 in SLC30A8 genes. 2 test, and data were expressed as odds ratios (ORs) with 95% confidence intervals (CIs). Values of p
format article
author Anna Viktorovna Zheleznyakova
Nadezhda Olegovna Lebedeva
Olga Konstantinovna Vikulova
Valery Vyacheslavovich Nosikov
Minara Shamkhalovna Shamkhalova
Marina Vladimirovna Shestakova
author_facet Anna Viktorovna Zheleznyakova
Nadezhda Olegovna Lebedeva
Olga Konstantinovna Vikulova
Valery Vyacheslavovich Nosikov
Minara Shamkhalovna Shamkhalova
Marina Vladimirovna Shestakova
author_sort Anna Viktorovna Zheleznyakova
title Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination
title_short Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination
title_full Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination
title_fullStr Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination
title_full_unstemmed Risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in NOS3, APOB, KCNJ11, TCF7L2 genes as compound effect of risk genotypes combination
title_sort risk of chronic kidney disease in type 2 diabetes determined by polymorphisms in nos3, apob, kcnj11, tcf7l2 genes as compound effect of risk genotypes combination
publisher Endocrinology Research Centre
publishDate 2014
url https://doaj.org/article/237d2a0144b948ea8e9f69bc14592804
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