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Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients
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)
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| Published in: | Free radical biology & medicine 2012-07, Vol.53 (1), p.60-63 |
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| creator | Choi, Siu-Wai Fai Yeung, Vincent Tok Benzie, Iris F.F. |
| description | 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) |
| doi_str_mv | 10.1016/j.freeradbiomed.2012.04.017 |
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► Activation of polymorphic HMOX-1 by oxidative stress is cytoprotective. ► Promoter GT(n)>25 reportedly blunts activation; this may affect outcome in type 2 diabetes mellitus (T2DM). ► We studied GT(n) and outcome in T2DM patients followed for up to 9 years. ► Oxidative stress and glycemic control were not different across GT(n) genotypes. ► GT(n) did not influence complication development.</description><identifier>ISSN: 0891-5849</identifier><identifier>EISSN: 1873-4596</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2012.04.017</identifier><identifier>PMID: 22583702</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>alleles ; antioxidants ; biomarkers ; blood ; Blood Glucose ; death ; Diabetes Complications - etiology ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetic complications ; DNA damage ; fasting ; Female ; Free radicals ; Genetic Predisposition to Disease ; Genotype ; genotyping ; glucose ; glycemic control ; glycohemoglobin ; GT repeats ; heme oxygenase (biliverdin-producing) ; Heme oxygenase-1 ; Heme Oxygenase-1 - genetics ; Humans ; lipids ; Male ; microsatellite repeats ; Microsatellite Repeats - genetics ; Middle Aged ; noninsulin-dependent diabetes mellitus ; Oxidative Stress ; patients ; Polymorphism, Genetic - genetics ; promoter regions ; Promoter Regions, Genetic - genetics ; risk ; Risk Factors ; Type 2 diabetes</subject><ispartof>Free radical biology & medicine, 2012-07, Vol.53 (1), p.60-63</ispartof><rights>2012 Elsevier Inc.</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-47999bc3ab1847d80171f92117fe74cc0fae3bb620a0686c492fc8bfcb0aaf83</citedby><cites>FETCH-LOGICAL-c407t-47999bc3ab1847d80171f92117fe74cc0fae3bb620a0686c492fc8bfcb0aaf83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22583702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Choi, Siu-Wai</creatorcontrib><creatorcontrib>Fai Yeung, Vincent Tok</creatorcontrib><creatorcontrib>Benzie, Iris F.F.</creatorcontrib><title>Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>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 2DM), and better glycemic control and outcome, but data are conflicting. We investigated GT(n) in type 2DM 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.
► Activation of polymorphic HMOX-1 by oxidative stress is cytoprotective. ► Promoter GT(n)>25 reportedly blunts activation; this may affect outcome in type 2 diabetes mellitus (T2DM). ► We studied GT(n) and outcome in T2DM patients followed for up to 9 years. ► Oxidative stress and glycemic control were not different across GT(n) genotypes. ► GT(n) did not influence complication development.</description><subject>alleles</subject><subject>antioxidants</subject><subject>biomarkers</subject><subject>blood</subject><subject>Blood Glucose</subject><subject>death</subject><subject>Diabetes Complications - etiology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetic complications</subject><subject>DNA damage</subject><subject>fasting</subject><subject>Female</subject><subject>Free radicals</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>genotyping</subject><subject>glucose</subject><subject>glycemic control</subject><subject>glycohemoglobin</subject><subject>GT repeats</subject><subject>heme oxygenase (biliverdin-producing)</subject><subject>Heme oxygenase-1</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Humans</subject><subject>lipids</subject><subject>Male</subject><subject>microsatellite repeats</subject><subject>Microsatellite Repeats - genetics</subject><subject>Middle Aged</subject><subject>noninsulin-dependent diabetes mellitus</subject><subject>Oxidative Stress</subject><subject>patients</subject><subject>Polymorphism, Genetic - genetics</subject><subject>promoter regions</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>risk</subject><subject>Risk Factors</subject><subject>Type 2 diabetes</subject><issn>0891-5849</issn><issn>1873-4596</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqNkcFu1DAQhi0EotvCK4AlLhw2y9hxEkecqqq0SJU4UM6W44wXr5I42N4VeQMeG0fbHrhxskbz_b9n_iHkA4MdA1Z_OuxsQAy675wfsd9xYHwHYgeseUE2TDZlIaq2fkk2IFtWVFK0F-QyxgMAiKqUr8kF55UsG-Ab8uceR6T-97LHSUekozPBR51wGFxCOvthGX2Yf7o4bjPmep3cCWlMAWPc0v2wGMwaavyUgh-2VE99LsZ5cCajfqI9nnDw84hTom6iaZmRcto73WHCSOdM5VZ8Q15ZPUR8-_Rekccvt48398XDt7uvN9cPhRHQpEI0bdt2ptQdk6LpZV6a2ZYz1lhshDFgNZZdV3PQUMvaiJZbIztrOtDayvKKfDzbzsH_OmJManTR5G31hP4YFYPsxQXUkNHPZ3RNJAa0ag5u1GHJkFovoQ7qn0uo9RIKhMpDZfW7p4-O3dp71j5Hn4H3Z8Bqr_Q-uKh-fM8OFQAr67ZaidszgTmPk8OgoslZGexdQJNU791_jfIXla6u2A</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Choi, Siu-Wai</creator><creator>Fai Yeung, Vincent Tok</creator><creator>Benzie, Iris F.F.</creator><general>Elsevier Inc</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20120701</creationdate><title>Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients</title><author>Choi, Siu-Wai ; Fai Yeung, Vincent Tok ; Benzie, Iris F.F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c407t-47999bc3ab1847d80171f92117fe74cc0fae3bb620a0686c492fc8bfcb0aaf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>alleles</topic><topic>antioxidants</topic><topic>biomarkers</topic><topic>blood</topic><topic>Blood Glucose</topic><topic>death</topic><topic>Diabetes Complications - etiology</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetic complications</topic><topic>DNA damage</topic><topic>fasting</topic><topic>Female</topic><topic>Free radicals</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>genotyping</topic><topic>glucose</topic><topic>glycemic control</topic><topic>glycohemoglobin</topic><topic>GT repeats</topic><topic>heme oxygenase (biliverdin-producing)</topic><topic>Heme oxygenase-1</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Humans</topic><topic>lipids</topic><topic>Male</topic><topic>microsatellite repeats</topic><topic>Microsatellite Repeats - genetics</topic><topic>Middle Aged</topic><topic>noninsulin-dependent diabetes mellitus</topic><topic>Oxidative Stress</topic><topic>patients</topic><topic>Polymorphism, Genetic - genetics</topic><topic>promoter regions</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>risk</topic><topic>Risk Factors</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Siu-Wai</creatorcontrib><creatorcontrib>Fai Yeung, Vincent Tok</creatorcontrib><creatorcontrib>Benzie, Iris F.F.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Siu-Wai</au><au>Fai Yeung, Vincent Tok</au><au>Benzie, Iris F.F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2012-07-01</date><risdate>2012</risdate><volume>53</volume><issue>1</issue><spage>60</spage><epage>63</epage><pages>60-63</pages><issn>0891-5849</issn><eissn>1873-4596</eissn><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 2DM), and better glycemic control and outcome, but data are conflicting. We investigated GT(n) in type 2DM 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.
► Activation of polymorphic HMOX-1 by oxidative stress is cytoprotective. ► Promoter GT(n)>25 reportedly blunts activation; this may affect outcome in type 2 diabetes mellitus (T2DM). ► We studied GT(n) and outcome in T2DM patients followed for up to 9 years. ► Oxidative stress and glycemic control were not different across GT(n) genotypes. ► GT(n) did not influence complication development.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22583702</pmid><doi>10.1016/j.freeradbiomed.2012.04.017</doi><tpages>4</tpages></addata></record> |
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| subjects | alleles antioxidants biomarkers blood Blood Glucose death Diabetes Complications - etiology Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - physiopathology Diabetic complications DNA damage fasting Female Free radicals Genetic Predisposition to Disease Genotype genotyping glucose glycemic control glycohemoglobin GT repeats heme oxygenase (biliverdin-producing) Heme oxygenase-1 Heme Oxygenase-1 - genetics Humans lipids Male microsatellite repeats Microsatellite Repeats - genetics Middle Aged noninsulin-dependent diabetes mellitus Oxidative Stress patients Polymorphism, Genetic - genetics promoter regions Promoter Regions, Genetic - genetics risk Risk Factors Type 2 diabetes |
| title | Heme oxygenase microsatellite polymorphism, oxidative stress, glycemic control, and complication development in type 2 diabetes patients |
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