scholarly journals Analysis of Uncoupling Protein 1 and β3-adrenergic Receptor Single Nucleotide Polymorphisms in Saudi Population with Type 2 Diabetes Mellitus

2020 ◽  
Vol 8 (A) ◽  
pp. 699-705
Author(s):  
Fathy М. Elfasakhany ◽  
Abdulah M. Karawagh ◽  
Shahid S. Siddiqui ◽  
Magdi A. Eldamarawi

BACKGROUND: Uncoupling proteins (UCP) and β3-adrenergic receptor (ADRB3) gene polymorphism have been implicated in the susceptibility to type 2 diabetes mellitus (T2DM) but the results are inconsistent and inconclusive. AIM: The aim was to investigate the relationship between -3826A/G (rs1800592) of UCP 1 and ADRB3 Trp64Arg (C/T) (rs4994) gene polymorphism and the incidence of T2DM among Saudis. METHODS: Genotyping of both UCP1 and ADRB3 genes was carried out in 110 healthy controls and 108 unrelated Saudis with T2DM using polymerase chain reaction-based restriction fragment length polymorphism. RESULTS: The genotype and allele frequencies of the UCP1 gene did not differ significantly between diabetic subjects and controls (p > 0.05). However, the CT genotype and the T allele of ADRB3 were higher in diabetic subjects compared with the controls while the CC genotype and C allele were higher in the controls relative to the diabetic subjects (Odds ratios [OR]: 7.85, 95% confidence interval [CI]: 4.23–14.59, p < 0.001 and OR: 7.434 95% CI: 4.026–13.39, p < 0.001, respectively). CONCLUSION: The UCP1 -3826A/G polymorphism may not be associated with the susceptibility to T2DM among Saudis while T allele of ADRB3 may be related to the risk of T2DM, whereas the CC genotype and C allele may confer protection to T2DM.

2006 ◽  
Vol 7 (1) ◽  
Author(s):  
Michele Pinelli ◽  
Manuela Giacchetti ◽  
Fabio Acquaviva ◽  
Sergio Cocozza ◽  
Giovanna Donnarumma ◽  
...  

2019 ◽  
Vol 15 (6) ◽  
pp. 446-455
Author(s):  
Marry-ann Ntanyane Phasha ◽  
Prashilla Soma ◽  
Etheresia Pretorius ◽  
Alia Phulukdaree

The prevalence of type 2 diabetes mellitus (T2DM) has quadrupled within three decades since 1980, affecting 422 million adults in 2016. It remains one of the most common noncommunicable chronic diseases and the underlying risk factor for cardiovascular diseases worldwide. There are different underlying mechanisms that play a role in the development of pathologies associated with the disease such as hyperglycaemia, oxidative stress, obesity, inflammation and hypercoagulation; each of which are interlinked. Hyperglycaemia, oxidative stress and obesity play a huge role in the activation of inflammation and coagulation. Activation of inflammatory pathways increases the production of thrombin which predisposes the development of thrombotic related diseases. One of the factors that contribute to the increase of thrombin is the impairment of the fibrinolysis process due to decreased expression of tissue-plasminogen activator (tPA) by increased levels of plasminogen activator inhibitor-1 (PAI-1). Coagulation factor XIII (FXIII), a transglutaminase that is composed of subunits A and B (FXIII-A2B2), is essential for the last step of fibrin clot formation in the coagulation pathway. Genetic variation of FXIII-A in the form of single nucleotide polymorphisms (SNPs) alters the activity of FXIII, altering clot properties which influence disease outcomes. This review discusses the link between underlying mechanisms of T2DM, well known FXIII-A variants and coagulation.


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