PMID- 30900957
OWN - NLM
STAT- MEDLINE
DCOM- 20200330
LR  - 20221207
IS  - 2474-0896 (Electronic)
IS  - 0967-4845 (Linking)
VI  - 76
IP  - 4
DP  - 2019 Oct
TI  - Interaction of antioxidant gene variants and susceptibility to type 2 diabetes 
      mellitus.
PG  - 166-171
LID - 10.1080/09674845.2019.1595869 [doi]
AB  - Background: Diabetes is the seventh most common disease leading to death with a 
      global estimate of 425 million diabetics, expected to be 629 million in 2045. The 
      role of reactive metabolites and antioxidants, such as glutathione, glutathione 
      peroxidase, superoxide dismutase and catalase in type 2 diabetes mellitus (T2DM) 
      provides an opportunity for identifying gene variants and risk genotypes. We 
      hypothesised that certain antioxidant gene-gene interactions are linked with T2DM 
      and can model disease risk prediction.Materials and methods: Genotyping of single 
      nucleotide polymorphisms (SNPs) in antioxidant genes for glutathione (GST), 
      glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) was 
      performed in 558 T2DMs and 410 age and sex matched healthy controls by polymerase 
      chain reaction-restriction fragment length polymorphism (PCR-RFLP), routine lab 
      indices by standard techniques.Results: The null/null allele combination of 
      GSTM1del and GSTT1del increased disease risk up to 1.7-fold. The combination of 
      SNPs in GSTM1del, GSTT1del, GSTP1 + 313A/G and in CAT-21A/T, SOD2 + 47C/T, GPx1 + 
      599C/T increased the risk of diabetes 13.5 and 2.1-fold, respectively. 
      Interaction of SNPs GSTM1del, GSTT1del, GSTP1 + 313A/G (105Ile/Val), CAT-21A/T, 
      SOD2 + 47C/T, GPx1 + 599C/T were significantly linked with disease risk >5 x 
      10(3) fold.Conclusion: As the number of gene combinations increase, there is a 
      rise in the odds ratio of disease risk, suggesting that gene-gene interaction 
      plays an important role in T2DM susceptibility. Individuals who possess the 
      GSTM1del, GSTT1del, GSTP1 105I/V(+313A/G), CAT-21A/T, SOD2 + 47C/T and GPx1 + 
      599C/T are at very high risk of developing T2DM.
FAU - Banerjee, M
AU  - Banerjee M
AD  - Molecular & Human Genetics Laboratory, Department of Zoology, University of 
      Lucknow, Lucknow, Uttar Pradesh, India.
FAU - Vats, P
AU  - Vats P
AD  - Molecular & Human Genetics Laboratory, Department of Zoology, University of 
      Lucknow, Lucknow, Uttar Pradesh, India.
FAU - Kushwah, A S
AU  - Kushwah AS
AD  - Molecular & Human Genetics Laboratory, Department of Zoology, University of 
      Lucknow, Lucknow, Uttar Pradesh, India.
AD  - Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, 
      Uttar Pradesh, India.
FAU - Srivastava, N
AU  - Srivastava N
AD  - Department of Physiology, King George's Medical University, Lucknow, Uttar 
      Pradesh, India.
LA  - eng
PT  - Journal Article
DEP - 20190521
PL  - Switzerland
TA  - Br J Biomed Sci
JT  - British journal of biomedical science
JID - 9309208
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 1.15.1.1 (superoxide dismutase 2)
RN  - EC 2.5.1.- (glutathione S-transferase T1)
RN  - EC 2.5.1.18 (Glutathione Transferase)
RN  - EC 2.5.1.18 (glutathione S-transferase M1)
RN  - EC 1.11.1.9 (Glutathione Peroxidase GPX1)
RN  - EC 1.11.1.9 (GPX1 protein, human)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - Case-Control Studies
MH  - Catalase/*genetics
MH  - Diabetes Mellitus, Type 2/diagnosis/*genetics/physiopathology
MH  - *Epistasis, Genetic
MH  - Female
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease
MH  - Glutathione Peroxidase/*genetics
MH  - Glutathione Transferase/*genetics
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Restriction Fragment Length
MH  - Prognosis
MH  - Risk
MH  - Superoxide Dismutase/*genetics
MH  - Glutathione Peroxidase GPX1
OTO - NOTNLM
OT  - Type 2 diabetes mellitus
OT  - antioxidants
OT  - gene variants
OT  - gene-gene interaction
OT  - susceptibility
EDAT- 2019/03/23 06:00
MHDA- 2020/03/31 06:00
CRDT- 2019/03/23 06:00
PHST- 2019/03/23 06:00 [pubmed]
PHST- 2020/03/31 06:00 [medline]
PHST- 2019/03/23 06:00 [entrez]
AID - 10.1080/09674845.2019.1595869 [pii]
AID - 10.1080/09674845.2019.1595869 [doi]
PST - ppublish
SO  - Br J Biomed Sci. 2019 Oct;76(4):166-171. doi: 10.1080/09674845.2019.1595869. Epub 
      2019 May 21.