scholarly journals Potential role of the ABCG2-Q141K polymorphism in type 2 diabetes

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260957
Author(s):  
Edit Szabó ◽  
Anna Kulin ◽  
Orsolya Mózner ◽  
László Korányi ◽  
Botond Literáti-Nagy ◽  
...  

Type 2 diabetes mellitus (T2DM) is a complex metabolic disease and variations in multispecific membrane transporter functions may affect T2DM development, complications or treatment. In this work we have analyzed the potential effects of a major polymorphism, the Q141K variant of the ABCG2 transporter in T2DM. The ABCG2 protein is a multispecific xeno- and endobiotic transporter, affecting drug metabolism and playing a key role in uric acid extrusion. The ABCG2-Q141K variant, with reduced expression level and function, is present in 15–35% of individuals, depending on the genetic background of the population, and has been shown to significantly affect gout development. Several other diseases, including hypertension, chronic renal failure, and T2DM have also been reported to be associated with high serum uric acid levels, suggesting that ABCG2 may also play a role in these conditions. In this work we have compared relatively small cohorts (n = 203) of T2DM patients (n = 99) and healthy (n = 104) individuals regarding the major laboratory indicators of T2DM and determined the presence of the SNP rs2231142 (C421A), resulting the ABCG2-Q141K protein variant. We found significantly higher blood glucose and HbA1c levels in the T2DM patients carrying the ABCG2-Q141K variant. These findings may emphasize the potential metabolic role of ABCG2 in T2DM and indicate that further research should explore how prevention and treatment of this disease may be affected by the frequent polymorphism of ABCG2.

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
N. Papanas ◽  
M. Demetriou ◽  
N. Katsiki ◽  
K. Papatheodorou ◽  
D. Papazoglou ◽  
...  

The aim of this paper was to assess serum uric acid (SUA) levels in patients with type 2 diabetes mellitus (T2DM) with or without sudomotor dysfunction (evaluated by the Neuropad test). We included 36 T2DM patients with sudomotor dysfunction (group A: mean age63.1±2.6years) and 40 age-, gender-, renal function- and T2DM duration-matched patients without sudomotor dysfunction (group B: mean age62.1±3.1years). SUA was significantly higher in group A (P<0.001). There was a significant correlation between SUA and Neuropad time to colour change in both groups (group A:rs=0.819,P<0.001; group B:rs=0.774,P<0.001). There was also a significant positive correlation between SUA and CRP in both groups (group A:rs=0.947,P<0.001; group B:rs=0.848,P<0.001). In conclusion, SUA levels were higher in T2DM patients with sudomotor dysfunction than those without this complication. The potential role of SUA in sudomotor dysfunction merits further study.


2014 ◽  
Vol 6 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Kentaro Tanaka ◽  
Shigeko Hara ◽  
Masakazu Hattori ◽  
Ken Sakai ◽  
Yukiko Onishi ◽  
...  

Diabetes Care ◽  
2008 ◽  
Vol 31 (9) ◽  
pp. e68-e68 ◽  
Author(s):  
G. Lippi ◽  
G. Targher ◽  
M. Montagnana ◽  
G. L. Salvagno ◽  
G. C. Guidi

2013 ◽  
Vol 41 (3) ◽  
pp. 797-801 ◽  
Author(s):  
Timothy J. Pullen ◽  
Guy A. Rutter

The progression of Type 2 diabetes is accompanied by diminishing islet β-cell mass and function. It has been proposed that β-cells are lost not only through apoptosis, but also by dedifferentiating into progenitor-like cells. There is therefore much interest in the mechanisms which define and maintain β-cell identity. The advent of genome-wide analyses of chromatin modifications has highlighted the role of epigenetic factors in determining cell identity. There is also evidence from both human populations and animal models for an epigenetic component in susceptibility to Type 2 diabetes. The mechanisms responsible for defining the epigenetic landscape in individual cell types are poorly understood, but there is growing evidence of a role for lncRNAs (long non-coding RNAs) in this process. In the present paper, we discuss some of the mechanisms through which lncRNAs may contribute to β-cell identity and Type 2 diabetes risk.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S574-S574
Author(s):  
Steven J Prior

Abstract Nearly three-fourths of adults over 65 year of age are affected by impaired glucose tolerance or type 2 diabetes. Both aging and inactivity contribute to the numerous skeletal muscle changes that occur with insulin resistance and type 2 diabetes. These changes include reduced capillarization that can impaired glucose uptake and substrate delivery, resulting in metabolic abnormalities and metabolic inflexibility. These changes may ultimately contribute to reduced delivery of oxygen, nutrients, and hormones to the muscles leading to impairments in metabolism, muscle mass, and function. We will discuss current research on the role of vascular impairments and reduced skeletal muscle capillarization in the development of impaired muscle metabolism, fitness and function. Finally, we will discuss how exercise training may reverse these declines.


2006 ◽  
Vol 8 (27) ◽  
pp. 1-12 ◽  
Author(s):  
Francis Vasseur ◽  
David Meyre ◽  
Philippe Froguel

Adiponectin, a protein exclusively secreted by adipose tissue but present at low levels in obesity, is now widely recognised as a key determinant of insulin sensitivity and of protection against obesity-associated metabolic syndrome. In this review we explain how genetic findings have contributed to a better understanding of the physiological role of adiponectin in humans. The adiponectin-encoding gene, ADIPOQ (ACDC), is very polymorphic: many frequent exonic synonymous, intronic and promoter single-nucleotide polymorphisms (SNPs) have been identified, as well as a few rare exonic amino acid substitutions. Several of these variations additively contribute to the modulation of adiponectin level and function, and associate with insulin sensitivity, type 2 diabetes and vascular complications of obesity.


Diabetes Care ◽  
2007 ◽  
Vol 31 (2) ◽  
pp. 361-362 ◽  
Author(s):  
A. Dehghan ◽  
M. van Hoek ◽  
E. J.G. Sijbrands ◽  
A. Hofman ◽  
J. C.M. Witteman

2018 ◽  
Vol 21 (4) ◽  
pp. 277-282
Author(s):  
Deasy Putri Sukarno ◽  
Muhammad Hamdan ◽  
Fidiana Fidiana ◽  
Fadil Fadil ◽  
Mudjiani Basuki

Background: The increased serum uric acid (SUA) levels have been linked to macro vascular disease in Type 2 Diabetes Melitus. The correlation between serum uric acid levels and diabetic peripheral neuropathy has not been addressed properly. Objective: The aim of this study was to determine the correlation between high serum uric acid levels and diabetic peripheral neuropathy. Methods: This was a case-control design study and the sampling was done consecutively by following the inclusion and the exclusion criteria. The diabetic peripheral neuropathy was evaluated using Electroneuromyography (EMNG) and the serum were taken for uric acid level examination. Chi square test was used for the correlation analysis. Result: Thirty subjects were enrolled and divided into an experimental group of 15 subjects and a control group of 15 subjects as well. We found that the diabetic peripheral neuropathy did not show a significant correlation with high serum uric acid levels, p=0,136 and OR 3,143 (CI 95% 0,681-14,503). Conclusions: There was no correlation between high serum uric acid levels with diabetic peripheral neuropathy.


Sign in / Sign up

Export Citation Format

Share Document