Malondialdehyde but Not Methylglyoxal Impairs Insulin Signaling, NO Production, and Endothelial Barrier
| Autor: | Alexander V. Vorotnikov, M. V. Samsonov, V. Z. Lankin, V. P. Shirinsky, N. V. Podkuychenko |
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| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
endocrine system diseases biology Insulin medicine.medical_treatment Methylglyoxal Biophysics nutritional and metabolic diseases Cell Biology medicine.disease biology.organism_classification Malondialdehyde Biochemistry Umbilical vein chemistry.chemical_compound Insulin receptor Endocrinology chemistry Enos Internal medicine medicine biology.protein Endothelial dysfunction skin and connective tissue diseases Protein kinase B |
| Zdroj: | Biochemistry (Moscow), Supplement Series A: Membrane and Cell Biology. 15:195-200 |
| ISSN: | 1990-7494 1990-7478 |
| DOI: | 10.1134/s1990747821030089 |
| Popis: | Dyslipidemia and hyperglycemia portray “cause-and-consequence” of type 2 diabetes mellitus (T2DM). They are linked to malondialdehyde (MDA) and methylglyoxal (MGO) generation that result from membrane lipid peroxidation and oxidative glucose conversions. We compared the effects of exogenous MDA and MGO on human umbilical vein endothelial cells and found that MDA but not MGO impairs insulin activation of PI3-kinase pathway, NO production, and endothelial barrier capacity. MDA abolished insulin activation of Akt and eNOS but not that of IRS. These results substantiate the hypothesis that MDA may be involved in endothelial dysfunction as an early event in the development of T2DM. |
| Databáze: | OpenAIRE |
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