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.
We conclude that the GLUT1 gene is very unlikely to play a major role in the aetiology of NIDDM, although an accessory role cannot be excluded, and studies of the gene sequence should help to clarify this question.
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.
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.
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.
This joint analysis suggests that GLUT1 polymorphism may contribute to susceptibility to type 2 diabetes in some populations, and especially in overweight/obese women.
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.
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.
The present study does not support the hypothesis that genetic variation within the GLUT1 or GLUT4 gene loci may be responsible for familial susceptibility to Type 2 diabetes.
The finding of an association between polymorphic markers at the GLUT1 transporter and NIDDM suggests that this locus may contribute to the inherited susceptibility to the disease in this Italian population.
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.
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.
Restriction site polymorphisms at the human HepG2 glucose transporter gene locus in Caucasian and west Indian subjects with non-insulin-dependent diabetes mellitus.
Linkage of GLUT1 and NIDDM was strongly and significantly rejected under all models, with total (pooled) LOD scores of -5.7 to -8.9, indicating > 500,000:1 odds against linkage.
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).
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.
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.