Please use this identifier to cite or link to this item: https://doi.org/10.1136/bmjdrc-2019-000945
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dc.titleHeredity of type 2 diabetes confers increased susceptibility to oxidative stress and inflammation
dc.contributor.authorBaig, Sonia
dc.contributor.authorShabeer, Muhammad
dc.contributor.authorParvaresh Rizi, Ehsan
dc.contributor.authorAgarwal, Madhur
dc.contributor.authorLee, Michelle H
dc.contributor.authorOoi, Delicia Shu Qin
dc.contributor.authorChia, Chelsea
dc.contributor.authorAung, Nweni
dc.contributor.authorNg, Geelyn
dc.contributor.authorTeo, Yvonne
dc.contributor.authorChhay, Vanna
dc.contributor.authorMagkos, Faidon
dc.contributor.authorVidal-Puig, Antonio
dc.contributor.authorSeet, Raymond CS
dc.contributor.authorToh, Sue-Anne
dc.date.accessioned2020-02-03T06:46:08Z
dc.date.available2020-02-03T06:46:08Z
dc.date.issued2020-01
dc.identifier.citationBaig, Sonia, Shabeer, Muhammad, Parvaresh Rizi, Ehsan, Agarwal, Madhur, Lee, Michelle H, Ooi, Delicia Shu Qin, Chia, Chelsea, Aung, Nweni, Ng, Geelyn, Teo, Yvonne, Chhay, Vanna, Magkos, Faidon, Vidal-Puig, Antonio, Seet, Raymond CS, Toh, Sue-Anne (2020-01). Heredity of type 2 diabetes confers increased susceptibility to oxidative stress and inflammation. BMJ Open Diabetes Research & Care 8 (1) : e000945-e000945. ScholarBank@NUS Repository. https://doi.org/10.1136/bmjdrc-2019-000945
dc.identifier.issn2052-4897
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/164246
dc.description.abstract<jats:sec><jats:title>Introduction and objective</jats:title><jats:p>Heredity of type 2 diabetes mellitus (T2DM) is associated with greater risk for developing T2DM. Thus, individuals who have a first-degree relative with T2DM (FDRT) provide a natural model to study factors of susceptibility towards development of T2DM, which are poorly understood. Emerging key players in T2DM pathophysiology such as adverse oxidative stress and inflammatory responses could be among possible mechanisms that predispose FDRTs to develop T2DM. Here, we aimed to examine the role of oxidative stress and inflammatory responses as mediators of this excess risk by studying dynamic postprandial responses in FDRTs.</jats:p></jats:sec><jats:sec><jats:title>Research design and methods</jats:title><jats:p>In this open-label case-control study, we recruited normoglycemic men with (n=9) or without (n=9) a family history of T2DM. We assessed plasma glucose, insulin, lipid profile, cytokines and F<jats:sub>2</jats:sub>-isoprostanes, expression levels of oxidative and inflammatory genes/proteins in circulating mononuclear cells (MNC), myotubes and adipocytes at baseline (fasting state), and after consumption of a carbohydrate-rich liquid meal or insulin stimulation.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Postprandial glucose and insulin responses were not different between groups. Expression of oxidant transcription factor NRF2 protein (p&lt;0.05 for myotubes) and gene (p<jats:sub>group</jats:sub>=0.002, p<jats:sub>time×group</jats:sub>=0.016), along with its target genes TXNRD1 (p<jats:sub>group</jats:sub>=0.004, p<jats:sub>time×group</jats:sub>=0.007), GPX3 (p<jats:sub>group</jats:sub>=0.011, p<jats:sub>time×group</jats:sub>=0.019) and SOD-1 (p<jats:sub>group</jats:sub>=0.046 and p<jats:sub>time×group</jats:sub>=0.191) was upregulated in FDRT-derived MNC after meal ingestion or insulin stimulation. Synergistically, expression of target genes of inflammatory transcription factor nuclear factor kappa B such as tumor necrosis factor alpha (p<jats:sub>group</jats:sub>=0.001, p<jats:sub>time×group</jats:sub>=0.007) was greater in FDRT-derived MNC than in non-FDRT-derived MNC after meal ingestion or insulin stimulation.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Our findings shed light on how heredity of T2DM confers increased susceptibility to oxidative stress and inflammation. This could provide early insights into the underlying mechanisms and future risk of FDRTs for developing T2DM and its associated complications.</jats:p></jats:sec>
dc.publisherBMJ
dc.sourceElements
dc.typeArticle
dc.date.updated2020-02-03T05:12:52Z
dc.contributor.departmentDEPT OF MEDICINE
dc.contributor.departmentDEPT OF PAEDIATRICS
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.description.doi10.1136/bmjdrc-2019-000945
dc.description.sourcetitleBMJ Open Diabetes Research & Care
dc.description.volume8
dc.description.issue1
dc.description.pagee000945-e000945
dc.published.statePublished
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