guest ::
| Home > Publications database > Effect of metformin treatment in patients with type 2 diabetes with respect to glyoxalase 1 activity in atherosclerotic lesions. > print |
| Home > Publications database > Effect of metformin treatment in patients with type 2 diabetes with respect to glyoxalase 1 activity in atherosclerotic lesions. > print |
| 001 | 143753 | ||
| 005 | 20240229121829.0 | ||
| 024 | 7 | _ | |a 10.1024/0301-1526/a000762 |2 doi |
| 024 | 7 | _ | |a pmid:30421661 |2 pmid |
| 024 | 7 | _ | |a 0251-1029 |2 ISSN |
| 024 | 7 | _ | |a 0301-1526 |2 ISSN |
| 024 | 7 | _ | |a 1664-2872 |2 ISSN |
| 024 | 7 | _ | |a altmetric:53432598 |2 altmetric |
| 037 | _ | _ | |a DKFZ-2019-01322 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Peters, Andreas S |b 0 |
| 245 | _ | _ | |a Effect of metformin treatment in patients with type 2 diabetes with respect to glyoxalase 1 activity in atherosclerotic lesions. |
| 260 | _ | _ | |a Göttingen [u.a.] |c 2019 |b Huber |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1582280448_27335 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a The enzyme glyoxalase1 (GLO1) is the main opponent in the degradation of the reactive metabolite methylglyoxal (MG), which by glycation of macromolecules is involved in atherogenesis. Reduced GLO1-activity in atherosclerotic tissue is known to be associated with diabetes. It has been shown that treatment of patients with type 2 diabetes with metformin leads to increased GLO1-activity in peripheral-blood-cells. The aim of this study was to evaluate whether metformin treatment increases GLO1-activity in atherosclerotic lesions of patients with type 2 diabetes.Patients with type 2 diabetes and carotid artery disease were included into the study prospectively. Type of diabetes-medication was documented upon admission along with demographic and clinical history. Using shock frozen endarterectomy-derived carotid artery plaques, GLO1-activity as well as protein expression was measured by a spectophotometric assay and western-blotting respectively.33 patients (76 % male, mean age 71 years) were included into the study and were divided according to treatment with metformin or not (15 vs. 18 patients). GLO1-activity was increased by the factor 1.36 when treated with metformin - however, not significantly (0.86 vs. 0.63 U/mg, p = 0.056). Normalisation of GLO1-activity onto GLO1-expression level lead to a significant increase by more than twofold (8.48 vs. 3.85, p = 0.044) while GLO1-protein levels did not differ significantly. GLO1-activity correlated positively with increasing HbA1c, especially under metformin treatment.Treatment with metformin in patients with type 2 diabetes is associated with enhanced GLO1-activity in atherosclerotic lesions. Regarding the macro- and microvascular complications in these patients further studies are needed to gain more insight into the effect of metformin on the GLO/MG system. |
| 536 | _ | _ | |a 323 - Metabolic Dysfunction as Risk Factor (POF3-323) |0 G:(DE-HGF)POF3-323 |c POF3-323 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 7 | |a Metformin |0 9100L32L2N |2 NLM Chemicals |
| 650 | _ | 7 | |a Lactoylglutathione Lyase |0 EC 4.4.1.5 |2 NLM Chemicals |
| 700 | 1 | _ | |a Wortmann, Markus |b 1 |
| 700 | 1 | _ | |a Fleming, Thomas H |b 2 |
| 700 | 1 | _ | |a Nawroth, Peter P |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Bruckner, Thomas |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Böckler, Dittmar |b 5 |
| 700 | 1 | _ | |a Hakimi, Maani |b 6 |
| 773 | _ | _ | |a 10.1024/0301-1526/a000762 |g Vol. 48, no. 2, p. 186 - 192 |0 PERI:(DE-600)2082843-3 |n 2 |p 186 - 192 |t Vasa |v 48 |y 2019 |x 1664-2872 |
| 909 | C | O | |p VDB |o oai:inrepo02.dkfz.de:143753 |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 3 |6 P:(DE-HGF)0 |
| 910 | 1 | _ | |a External Institute |0 I:(DE-HGF)0 |k Extern |b 4 |6 P:(DE-HGF)0 |
| 913 | 1 | _ | |a DE-HGF |l Herz-Kreislauf-Stoffwechselerkrankungen |1 G:(DE-HGF)POF3-320 |0 G:(DE-HGF)POF3-323 |2 G:(DE-HGF)POF3-300 |v Metabolic Dysfunction as Risk Factor |x 0 |4 G:(DE-HGF)POF |3 G:(DE-HGF)POF3 |b Gesundheit |
| 914 | 1 | _ | |y 2019 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0300 |2 StatID |b Medline |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0310 |2 StatID |b NCBI Molecular Biology Database |
| 915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b VASA : 2017 |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0200 |2 StatID |b SCOPUS |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0199 |2 StatID |b Clarivate Analytics Master Journal List |
| 915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0110 |2 StatID |b Science Citation Index |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)0150 |2 StatID |b Web of Science Core Collection |
| 915 | _ | _ | |a WoS |0 StatID:(DE-HGF)0111 |2 StatID |b Science Citation Index Expanded |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1110 |2 StatID |b Current Contents - Clinical Medicine |
| 915 | _ | _ | |a DBCoverage |0 StatID:(DE-HGF)1050 |2 StatID |b BIOSIS Previews |
| 915 | _ | _ | |a IF < 5 |0 StatID:(DE-HGF)9900 |2 StatID |
| 920 | 1 | _ | |0 I:(DE-He78)A170-20160331 |k A170 |l Molekulare Stoffwechselkontrolle |x 0 |
| 980 | _ | _ | |a journal |
| 980 | _ | _ | |a VDB |
| 980 | _ | _ | |a I:(DE-He78)A170-20160331 |
| 980 | _ | _ | |a UNRESTRICTED |
| Library | Collection | CLSMajor | CLSMinor | Language | Author |
|---|