File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1016/j.freeradbiomed.2012.04.017
- Scopus: eid_2-s2.0-84861633218
- PMID: 22583702
- WOS: WOS:000305857400007
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients
Title | Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients |
---|---|
Authors | |
Keywords | Oxidative stress Type 2 diabetes Diabetic complications Heme oxygenase-1 GT repeats Free radicals |
Issue Date | 2012 |
Citation | Free Radical Biology and Medicine, 2012, v. 53, n. 1, p. 60-63 How to Cite? |
Abstract | Heme oxygenase-1 (HMOX-1) is activated by oxidative stress, and gene responsiveness is reportedly determined by the number of dinucleotide (GT(n)) repeats in its highly polymorphic promoter region. Short (S; GT(n)<25) alleles reportedly associate with higher response, lower oxidative stress, lower risk of type 2 diabetes mellitus (type 2 DM), and better glycemic control and outcome, but data are conflicting. We investigated GT(n) in type 2 DM subjects (all ethnic Chinese) in relation to basal glycemic control, oxidative stress, and outcome during up to 9 years follow-up. Fasting blood from 418 type 2 DM subjects was collected at entry for GT(n) genotyping, glycated hemoglobin, glucose, lipids, and biomarkers of oxidative stress and antioxidants. A subset (n=368) was followed for up to 9 years for incident complications or death. GT(n) genotype distribution was 128, 182, and 108 for, respectively, S/S, S/L, and L/L. No significant differences in glycemic control, lipids, or oxidative stress were seen across genotypes. During follow-up, 168/368 subjects developed complications. No association was seen with GT(n). No difference in plasma HO-1 was seen between genotypes in a small substudy (S/S n=21 vs L/L n=23). Glycated hemoglobin and lymphocytic DNA damage was higher (p<0.05) at entry in the incident complications group. No other significant differences were seen in oxidative stress or antioxidants. Data do not support the postulated link between HMOX-1 microsatellite polymorphism and type 2 DM or the putative beneficial effect of the S allele on glycemic control, oxidative stress, or outcome in type 2 DM patients, at least in this particular population. © 2012 Elsevier Inc. |
Persistent Identifier | http://hdl.handle.net/10722/271468 |
ISSN | 2023 Impact Factor: 7.1 2023 SCImago Journal Rankings: 1.752 |
ISI Accession Number ID |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Choi, Siu Wai | - |
dc.contributor.author | Fai Yeung, Vincent Tok | - |
dc.contributor.author | Benzie, Iris F.F. | - |
dc.date.accessioned | 2019-07-02T07:16:09Z | - |
dc.date.available | 2019-07-02T07:16:09Z | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | Free Radical Biology and Medicine, 2012, v. 53, n. 1, p. 60-63 | - |
dc.identifier.issn | 0891-5849 | - |
dc.identifier.uri | http://hdl.handle.net/10722/271468 | - |
dc.description.abstract | Heme oxygenase-1 (HMOX-1) is activated by oxidative stress, and gene responsiveness is reportedly determined by the number of dinucleotide (GT(n)) repeats in its highly polymorphic promoter region. Short (S; GT(n)<25) alleles reportedly associate with higher response, lower oxidative stress, lower risk of type 2 diabetes mellitus (type 2 DM), and better glycemic control and outcome, but data are conflicting. We investigated GT(n) in type 2 DM subjects (all ethnic Chinese) in relation to basal glycemic control, oxidative stress, and outcome during up to 9 years follow-up. Fasting blood from 418 type 2 DM subjects was collected at entry for GT(n) genotyping, glycated hemoglobin, glucose, lipids, and biomarkers of oxidative stress and antioxidants. A subset (n=368) was followed for up to 9 years for incident complications or death. GT(n) genotype distribution was 128, 182, and 108 for, respectively, S/S, S/L, and L/L. No significant differences in glycemic control, lipids, or oxidative stress were seen across genotypes. During follow-up, 168/368 subjects developed complications. No association was seen with GT(n). No difference in plasma HO-1 was seen between genotypes in a small substudy (S/S n=21 vs L/L n=23). Glycated hemoglobin and lymphocytic DNA damage was higher (p<0.05) at entry in the incident complications group. No other significant differences were seen in oxidative stress or antioxidants. Data do not support the postulated link between HMOX-1 microsatellite polymorphism and type 2 DM or the putative beneficial effect of the S allele on glycemic control, oxidative stress, or outcome in type 2 DM patients, at least in this particular population. © 2012 Elsevier Inc. | - |
dc.language | eng | - |
dc.relation.ispartof | Free Radical Biology and Medicine | - |
dc.subject | Oxidative stress | - |
dc.subject | Type 2 diabetes | - |
dc.subject | Diabetic complications | - |
dc.subject | Heme oxygenase-1 | - |
dc.subject | GT repeats | - |
dc.subject | Free radicals | - |
dc.title | Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.freeradbiomed.2012.04.017 | - |
dc.identifier.pmid | 22583702 | - |
dc.identifier.scopus | eid_2-s2.0-84861633218 | - |
dc.identifier.volume | 53 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 60 | - |
dc.identifier.epage | 63 | - |
dc.identifier.eissn | 1873-4596 | - |
dc.identifier.isi | WOS:000305857400007 | - |
dc.identifier.issnl | 0891-5849 | - |