Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions
Background and Aims. Adipose tissue dysfunction results from many factors, including glycation-induced microvascular damages. We tested the usefulness of inhibiting methylglyoxal-induced glycation to adipose tissue microvasculature in this work, using the antioxidant and dicarbonyl scavenger drug py...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2013/690650 |
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| author | Tiago Rodrigues Paulo Matafome Daniela Santos-Silva Cristina Sena Raquel Seiça |
| author_facet | Tiago Rodrigues Paulo Matafome Daniela Santos-Silva Cristina Sena Raquel Seiça |
| author_sort | Tiago Rodrigues |
| collection | DOAJ |
| description | Background and Aims. Adipose tissue dysfunction results from many factors, including glycation-induced microvascular damages. We tested the usefulness of inhibiting methylglyoxal-induced glycation to adipose tissue microvasculature in this work, using the antioxidant and dicarbonyl scavenger drug pyridoxamine. Methods. A group of Wistar rats was treated daily with methylglyoxal (MG, 75 mg/Kg/day, 8 weeks). Half of this group was treated with pyridoxamine in the following 4 weeks (Pyr) (100 mg/Kg/day) and the other half did not have any further treatment (MG). A group of Wistar rats without MG treatment was used as control (C). Results. MG group showed decreased HDL cholesterol and increased plasma free fatty acids levels, what was reverted by pyridoxamine. MG also caused an increase of tissue CEL levels (glycation marker), as well as increased staining of PAS and Masson Trichrome-positive components. Pyridoxamine led to CEL and TGF-β levels similar to those observed in control rats and inhibited the accumulation of PAS and Masson Trichrome-positive components. MG caused a decrease of Bcl-2/Bax ratio (marker of apoptosis) and vWF staining (microvascular marker), what was partially reverted by the treatment with pyridoxamine. Conclusions. Preventing methylglyoxal-induced accumulation of glycated and fibrotic materials using pyridoxamine improves the microvascular lesions of the adipose tissue. |
| format | Article |
| id | doaj-art-81e29a46281b4a72859586f1804cc943 |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-81e29a46281b4a72859586f1804cc9432025-02-03T01:30:58ZengWileyJournal of Diabetes Research2314-67452314-67532013-01-01201310.1155/2013/690650690650Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular LesionsTiago Rodrigues0Paulo Matafome1Daniela Santos-Silva2Cristina Sena3Raquel Seiça4Laboratory of Physiology, Institute of Biomedical Research on Light and Image (IBILI), Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, PortugalLaboratory of Physiology, Institute of Biomedical Research on Light and Image (IBILI), Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, PortugalLaboratory of Physiology, Institute of Biomedical Research on Light and Image (IBILI), Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, PortugalLaboratory of Physiology, Institute of Biomedical Research on Light and Image (IBILI), Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, PortugalLaboratory of Physiology, Institute of Biomedical Research on Light and Image (IBILI), Faculty of Medicine, University of Coimbra, 3000-354 Coimbra, PortugalBackground and Aims. Adipose tissue dysfunction results from many factors, including glycation-induced microvascular damages. We tested the usefulness of inhibiting methylglyoxal-induced glycation to adipose tissue microvasculature in this work, using the antioxidant and dicarbonyl scavenger drug pyridoxamine. Methods. A group of Wistar rats was treated daily with methylglyoxal (MG, 75 mg/Kg/day, 8 weeks). Half of this group was treated with pyridoxamine in the following 4 weeks (Pyr) (100 mg/Kg/day) and the other half did not have any further treatment (MG). A group of Wistar rats without MG treatment was used as control (C). Results. MG group showed decreased HDL cholesterol and increased plasma free fatty acids levels, what was reverted by pyridoxamine. MG also caused an increase of tissue CEL levels (glycation marker), as well as increased staining of PAS and Masson Trichrome-positive components. Pyridoxamine led to CEL and TGF-β levels similar to those observed in control rats and inhibited the accumulation of PAS and Masson Trichrome-positive components. MG caused a decrease of Bcl-2/Bax ratio (marker of apoptosis) and vWF staining (microvascular marker), what was partially reverted by the treatment with pyridoxamine. Conclusions. Preventing methylglyoxal-induced accumulation of glycated and fibrotic materials using pyridoxamine improves the microvascular lesions of the adipose tissue.http://dx.doi.org/10.1155/2013/690650 |
| spellingShingle | Tiago Rodrigues Paulo Matafome Daniela Santos-Silva Cristina Sena Raquel Seiça Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions Journal of Diabetes Research |
| title | Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions |
| title_full | Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions |
| title_fullStr | Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions |
| title_full_unstemmed | Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions |
| title_short | Reduction of Methylglyoxal-Induced Glycation by Pyridoxamine Improves Adipose Tissue Microvascular Lesions |
| title_sort | reduction of methylglyoxal induced glycation by pyridoxamine improves adipose tissue microvascular lesions |
| url | http://dx.doi.org/10.1155/2013/690650 |
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