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SLC2A4 Expression and its Epigenetic Regulation as Biomarkers for Insulin Resistance Treatment in Diabetes Mellitus

表观遗传学 胰岛素抵抗 DNA甲基化 药物基因组学 医学 生物信息学 梅德林 糖尿病 内科学 内分泌学 生物 遗传学 药理学 基因表达 基因 生物化学
作者
João Victor Del Conti Esteves,Caio Yogi Yonamine,Ubiratan Fabres Machado
出处
期刊:Biomarkers in Medicine [Future Medicine]
卷期号:14 (6): 413-416 被引量:11
标识
DOI:10.2217/bmm-2019-0481
摘要

Biomarkers in MedicineVol. 14, No. 6 EditorialSLC2A4 expression and its epigenetic regulation as biomarkers for insulin resistance treatment in diabetes mellitusJoão V Esteves‡, Caio Y Yonamine‡ & Ubiratan F MachadoJoão V Esteves‡Department of Physiology & Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil, Caio Y Yonamine‡Department of Physiology & Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil & Ubiratan F Machado *Author for correspondence: Tel.: +55 113 091 7494; E-mail Address: ubiratan@icb.usp.brhttps://orcid.org/0000-0002-8237-2435Department of Physiology & Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, BrazilPublished Online:6 Apr 2020https://doi.org/10.2217/bmm-2019-0481AboutSectionsView ArticleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInReddit View articleKeywords: DNA methylationGLUT4H3K9me3histone PTMsmicroRNAspharmacogenomicskeletal muscleReferences1. 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Intra-uterine undernutrition amplifies age-associated glucose intolerance in pigs via altered DNA methylation at muscle GLUT4 promoter. Br. J. Nutr. 116(3), 390–401 (2016).Crossref, Medline, CAS, Google Scholar7. Smith JA, Kohn TA, Chetty AK, Ojuka EO. CaMK activation during exercise is required forhistone hyperacetylation and MEF2A binding at the MEF2 site on the Glut4 gene. Am. J. Physiol. Endocrinol. Metab. 295(3), E698–E704 (2008).Crossref, Medline, CAS, Google Scholar8. Yonamine CY, Alves-Wagner AB, Esteves JV et al. Diabetes induces tri-methylation at lysine 9 of histone 3 at Slc2a4 gene in skeletal muscle: A new target to improve glycemic control. Mol. Cell. Endocrinol. 481, 26–34 (2019).Crossref, Medline, CAS, Google Scholar9. Sabari BR, Zhang D, Allis CD, Zhao Y. Metabolic regulation of gene expression through histone acylations. Nat. Rev. Mol. Cell Biol. 18(2), 90–101 (2017).Crossref, Medline, CAS, Google Scholar10. Remsberg JR, Ediger BN, Ho WY et al. Deletion of histone deacetylase 3 in adult beta cells improves glucose tolerance via increased insulin secretion. Mol. Metab. 6(1), 30–37 (2016).Crossref, Medline, Google Scholar11. Yonamine CY, Pinheiro-Machado E, Michalani ML et al. Resveratrol improves glycemic control in Type 2 diabetic obese mice by regulating glucose transporter expression in skeletal muscle and liver. Molecules 22(7), E1180 (2017).Crossref, Medline, Google Scholar12. Kelly AD, Issa JJ. The promise of epigenetic therapy: reprogramming the cancer epigenome. Curr. Opin. Genet. Dev. 42, 68–77 (2017).Crossref, Medline, CAS, Google Scholar13. Esteves JV, Enguita FJ, Machado UF. MicroRNAs-mediated regulation of skeletal muscle GLUT4 expression and translocation in insulin resistance. J. Diabetes Res. 2017, 7267910 (2017).Crossref, Medline, Google Scholar14. Esteves JV, Yonamine CY, Pinto-Junior DC, Gerlinger-Romero F, Enguita FJ, Machado UF. Diabetes modulates microRNAs 29b-3p, 29c-3p, 199a-5p and 532–3p expression in muscle: possible role in GLUT4 and HK2 repression. Front. Endocrinol. (Lausanne) 9, 536 (2018).Crossref, Medline, Google Scholar15. Massart J, Sjögren RJO, Lundell LS et al. Altered miR-29 expression in Type 2 diabetes influences glucose and lipid metabolism in skeletal muscle. Diabetes 66(7), 1807–1818 (2017).Crossref, Medline, CAS, Google Scholar16. Song H, Ding L, Zhang S, Wang W. MiR-29 family members interact with SPARC to regulate glucose metabolism. Biochem. Biophys. Res. Commun. 497(2), 667–674 (2018).Crossref, Medline, CAS, Google Scholar17. Yang Y, Jiang H, Xiao L, Yang X. MicroRNA-33b-5p is overexpressed and inhibits GLUT4 by targeting HMGA2 in polycystic ovarian syndrome: an in vivo and in vitro study. Oncol. Rep. 39(6), 3073–3085 (2018).Medline, CAS, Google Scholar18. Chen T, Zhang Y, Liu Y et al. MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling. Aging (Albany NY) 11(18), 7510–7524 (2019).Crossref, Medline, CAS, Google Scholar19. Xiao D, Zhou T, Fu Y et al. MicroRNA-17 impairs glucose metabolism in insulin-resistant skeletal muscle via repressing glucose transporter 4 expression. Eur. J. Pharmacol. 838, 170–176 (2018).Crossref, Medline, CAS, Google Scholar20. US National Library of Medicine. ClinicalTrials.gov (2016). https://clinicaltrials.gov/ct2/show/study/NCT02826525Crossref, Google ScholarFiguresReferencesRelatedDetailsCited ByDNA methylation profile of liver of mice conceived by in vitro fertilization14 June 2021 | Journal of Developmental Origins of Health and Disease, Vol. 13, No. 3Genetic Polymorphisms and Their Interactions with the Risk Factors of Cardiovascular Diseases: Review Chapter6 April 2022Gene set enrichment analysis and ingenuity pathway analysis to identify biomarkers in Sheng-ji Hua-yu formula treated diabetic ulcersJournal of Ethnopharmacology, Vol. 285PPARG Hypermethylation as the First Epigenetic Modification in Newly Onset Insulin Resistance in Human Adipocytes9 June 2021 | Genes, Vol. 12, No. 6miR-335-5p aggravates type 2 diabetes by inhibiting SLC2A4 expressionBiochemical and Biophysical Research Communications, Vol. 558Estrogen and Glycemic Homeostasis: The Fundamental Role of Nuclear Estrogen Receptors ESR1/ESR2 in Glucose Transporter GLUT4 Regulation7 January 2021 | Cells, Vol. 10, No. 1 Vol. 14, No. 6 Follow us on social media for the latest updates Metrics Downloaded 106 times History Received 25 October 2019 Accepted 29 January 2020 Published online 6 April 2020 Published in print April 2020 Information© 2020 Future Medicine LtdKeywordsDNA methylationGLUT4H3K9me3histone PTMsmicroRNAspharmacogenomicskeletal muscleFinancial & competing interests disclosureThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.No writing assistance was utilized in the production of this manuscript.PDF download
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