Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Heredity of type 2 diabetes confers increased susceptibility to oxidative stress and inflammation

Baig S., Shabeer M., Parvaresh Rizi E., Agarwal M., Lee MH., Ooi DSQ.

Laboratory Study with a reported sample of 9 on Type 2 Diabetes, Chronic Inflammation, published in BMJ Open Diabetes Res Care (2020) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
BMJ Open Diabetes Res Care (2020)
Reported sample size
9
Source database
Europe PMC
PMID
32049633
PMCID
PMC7039582
DOI
10.1136/bmjdrc-2019-000945
Citations
20

Abstract (original English)

Introduction and objective 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. Research design and methods 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 2 -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. Results Postprandial glucose and insulin responses were not different between groups. Expression of oxidant transcription factor NRF2 protein (p group =0.002, p time×group =0.016), along with its target genes TXNRD1 (p group =0.004, p time×group =0.007), GPX3 (p group =

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
HumansDiabetes Mellitus, Type 2InflammationF2-IsoprostanesCase-Control StudiesHeredityOxidative StressMale

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research