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Putative role of polymorphisms in UCP1-3 genes for diabetic nephropathy.

Lindholm, Eero LU ; Klannemark, Mia LU ; Agardh, Elisabet LU ; Groop, Leif LU and Agardh, Carl-David LU (2004) In Journal of Diabetes and its Complications 18(2). p.103-107
Abstract
Increased production of reactive oxygen species (ROS) has been suggested as a cause of diabetic complications. Uncoupling proteins (UCPs) have been ascribed a role in reducing the formation of ROS, and genetic variation in genes encoding for UCPs could thus be putative candidate genes for diabetic nephropathy. To test this hypothesis we searched for association between the A→G (−3862) variant in UCP1, the insertion/deletion (I/D) polymorphism in exon 8 in UCP2, and the C→T (−55) polymorphism in UCP3 and diabetic nephropathy in 218 diabetic patients with normal urinary albumin excretion rate (AER), 216 with micro- or macroalbuminuria, and in 106 control subjects without a family history of diabetes. We did not find any association between... (More)
Increased production of reactive oxygen species (ROS) has been suggested as a cause of diabetic complications. Uncoupling proteins (UCPs) have been ascribed a role in reducing the formation of ROS, and genetic variation in genes encoding for UCPs could thus be putative candidate genes for diabetic nephropathy. To test this hypothesis we searched for association between the A→G (−3862) variant in UCP1, the insertion/deletion (I/D) polymorphism in exon 8 in UCP2, and the C→T (−55) polymorphism in UCP3 and diabetic nephropathy in 218 diabetic patients with normal urinary albumin excretion rate (AER), 216 with micro- or macroalbuminuria, and in 106 control subjects without a family history of diabetes. We did not find any association between the different polymorphisms and diabetic nephropathy, nor did we observe any difference in AER among carriers of different UCP1–3 genotypes. We could, however, confirm the reported association between BMI and the UCP3 −55 C→T polymorphism; patients carrying the T allele had higher BMI than patients homozygous for the C allele (26.4±4.2 vs. 25.3±4.3 kg/m2; P=.01). We conclude that studied polymorphisms in the UCP1–3 genes do not play a major role in the development of micro- or macroalbuminuria in Scandinavian diabetic patients. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Uncoupling proteins, Diabetes mellitus, Microalbuminuria, Polymorphisms
in
Journal of Diabetes and its Complications
volume
18
issue
2
pages
103 - 107
publisher
Elsevier
external identifiers
  • wos:000221457400004
  • scopus:2142708616
ISSN
1873-460X
DOI
10.1016/S1056-8727(03)00019-9
language
English
LU publication?
yes
id
5d21a508-c1c9-4416-b507-205a0c4b6560 (old id 123676)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15120704&dopt=Abstract
date added to LUP
2007-07-16 16:20:03
date last changed
2017-01-01 06:40:55
@article{5d21a508-c1c9-4416-b507-205a0c4b6560,
  abstract     = {Increased production of reactive oxygen species (ROS) has been suggested as a cause of diabetic complications. Uncoupling proteins (UCPs) have been ascribed a role in reducing the formation of ROS, and genetic variation in genes encoding for UCPs could thus be putative candidate genes for diabetic nephropathy. To test this hypothesis we searched for association between the A→G (−3862) variant in UCP1, the insertion/deletion (I/D) polymorphism in exon 8 in UCP2, and the C→T (−55) polymorphism in UCP3 and diabetic nephropathy in 218 diabetic patients with normal urinary albumin excretion rate (AER), 216 with micro- or macroalbuminuria, and in 106 control subjects without a family history of diabetes. We did not find any association between the different polymorphisms and diabetic nephropathy, nor did we observe any difference in AER among carriers of different UCP1–3 genotypes. We could, however, confirm the reported association between BMI and the UCP3 −55 C→T polymorphism; patients carrying the T allele had higher BMI than patients homozygous for the C allele (26.4±4.2 vs. 25.3±4.3 kg/m2; P=.01). We conclude that studied polymorphisms in the UCP1–3 genes do not play a major role in the development of micro- or macroalbuminuria in Scandinavian diabetic patients.},
  author       = {Lindholm, Eero and Klannemark, Mia and Agardh, Elisabet and Groop, Leif and Agardh, Carl-David},
  issn         = {1873-460X},
  keyword      = {Uncoupling proteins,Diabetes mellitus,Microalbuminuria,Polymorphisms},
  language     = {eng},
  number       = {2},
  pages        = {103--107},
  publisher    = {Elsevier},
  series       = {Journal of Diabetes and its Complications},
  title        = {Putative role of polymorphisms in UCP1-3 genes for diabetic nephropathy.},
  url          = {http://dx.doi.org/10.1016/S1056-8727(03)00019-9},
  volume       = {18},
  year         = {2004},
}