Putative role of polymorphisms in UCP1-3 genes for diabetic nephropathy.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/123676
- author
- Lindholm, Eero LU ; Klannemark, Mia LU ; Agardh, Elisabet LU ; Groop, Leif LU and Agardh, Carl-David LU
- organization
- publishing date
- 2004
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Endocrinology (013241500), Developmental biology (LUR000007), Ophthalmology (013242810), Diabetes and Endocrinology (013241530), Unit on Vascular Diabetic Complications (013241510)
- 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
- 2016-04-01 15:30:08
- date last changed
- 2024-01-10 16:00:34
@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}}, keywords = {{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 = {{https://lup.lub.lu.se/search/files/4406790/632953.pdf}}, doi = {{10.1016/S1056-8727(03)00019-9}}, volume = {{18}}, year = {{2004}}, }