Here we studied the possible role of these gasotransmitters in both murine and human type 2 diabetes (T2D) by mapping the expression pattern of neural nitric oxide synthase (nNOS), inducible NOS (iNOS), constitutive heme oxygenase (HO-2), and inducible HO (HO-1) in isolated pancreatic islets.
This pilot study analyzed whether a 3-month endurance training can affect iNOS protein and NO metabolite levels in the vastus lateralis muscle of insulin-independent T2DM men, thereby affecting the patients` glycemic control.
The allele-C and genotype-TC of NOS2rs2779248, allele-A and genotype-GA of NOS2rs1137933 and genotype-AA of NOS3 rs3918188 genetic polymorphisms might be the risk factors for increasing the susceptibility to T2DM.
Genetic variations in the NOS2 gene promoter and TLR4 coding sequence may lead to deleterious and protective effects, respectively, arising from altered function of the innate immune system in patients with T2DM.
We previously reported the association of the Z-2 allele of the promoter dinucleotide repeat in the Aldose reductase (ALR2) gene, the (CCTTT)₁₅ allele in the promoter of inductible nitric oxide synthase (iNOS) gene, and the (GT)₁₃ promoter polymorphism in the tumor necrosis factor β (TNFB) gene with an increased risk for diabetic retinopathy (DR), and the Gly82Ser polymorphism in the receptor for advanced glycation end products (RAGE) gene and the (GT)₉ allele of the TNFB gene with low-risk for DR in a hospital-based self-reported type 2 diabetes mellitus (T2DM) patients.
We therefore tested a 4-bp insertion/deletion (+/-) polymorphism 0.7 kb upstream of NOS2A for association with complications in type 2 diabetes patients, and also performed transient transfection experiments to examine the effect of this variant on promoter activity in kidney cells in culture.