Thus, these results strongly suggest that T2D is associated with alterations in GLUT1 expression in the cells of striated ducts with mitochondrial dysfunction, causing a hyperplastic process characterized by multiple oncocytic cysts.
In this study, we investigated the association between the solute carrier family 2 facilitated glucose transporter member 1 (SLC2A1) <i>HaeIII</i> polymorphism and DN in Korean patients with type 2 diabetes mellitus (T2DM) according to disease duration.
An association study was conducted to investigate the relation between 14 variants of glucose transporter 1 gene (SLC2A1) and the risk of type 2 diabetes (T2DM) leading to nephropathy.
This interest is related to the importance of the GLUTs as archetypical membrane transport facilitators, as key limiters of the supply of glucose to cell metabolism, as targets of cell insulin and exercise signalling and of regulated membrane traffic, and as potential drug targets to combat cancer and metabolic diseases such as type 2 diabetes and obesity.
WSF-P-1 also activates GLUT1-mediated glucose uptake in 3T3-L1 adipocytes, making it a potential drug candidate for the treatment of type 2 diabetes, obesity, and other obesity-related metabolic diseases.
In contrast, a recent study showed that a synthetic inhibitor of SIRT6 improved glucose tolerance in a type 2 diabetes mouse model, associated with increased glycolysis and the expression of glucose transporter GLUT-1 and 4 in skeletal muscle, providing proof-of-concept evidence of SIRT6 inhibition as a treatment for diabetes.
As far as the authors are concerned, this study is the first one aiming at evaluating the probable effects of solute carrier family 2 facilitated glucose transporter member 1 (SLC2A1) HaeIII polymorphism on clinical and laboratory outcomes of Kurdish patients with type 2 diabetes mellitus.
Several SNPs of SLC2A1 (solute carrier family 2 [facilitated glucose transporter] member 1) showed association with NAFLD, but not with T2DM, being the haplotype containing the minor allele of SLC2A1 sequence related to the susceptibility to develop NAFLD.
A comprehensive literature search of electronic databases was conducted to obtain articles focused on the relationship between the GLUT1rs841853 polymorphism and T2DM, followed by a systemic meta-analysis.
The aim of this study was the estimation of insulin resistance indicators and the quantitative expression of GLUT-1, GLUT-3 and GLUT-4 on peripheral blood lymphocytes in prediabetic subjects and persons with a positive family history of type 2 diabetes during 24 months of observation.
PED (phosphoprotein enriched in diabetes) is a 15 kDa protein involved in many cellular pathways and human diseases including type II diabetes and cancer.
This study was undertaken to quantify the expression of muscle GLUT in type 2 diabetes and to determine if treatment with an insulin-enhancing thiazolidenedione drug, pioglitazone, would alter its expression.
In summary, 1) skeletal muscle tissue GLUT1 protein expression is reduced in type 2 diabetes and could contribute to impaired basal leg glucose uptake; and 2) elevated rates of basal whole body glucose uptake in type 2 diabetes are due to uptake in tissues other than skeletal muscle.
The results of this study in Caucasian patients with type 2 diabetes indicate that the XbaI(-) allele in the GLUT1 gene protects against the development of diabetic nephropathy.
However, the strong association between the GLUT1 gene and NIDDM, together with the recent family studies showing linkage between chromosome 1p and NIDDM warrant further studies on this chromosomal region.
We conclude that GLUT1 loci did not contribute significantly to type 2 diabetes in this cohort and is not a determinant for cardiovascular risk factors or chronic microangiopathic complications associated with type 2 diabetes.
Increased basal GLUT1 content in the plasma membrane was also observed in skeletal muscle of 4 NIDDM and 3 non-diabetic obese individuals (p < 0.05 vs the lean non diabetic subjects).