Abstract
The aim of the present study was to investigate the correlation between the adiponectin gene single nucleotide polymorphism (SNP)45 T/G and long-term oxidative stress in type II diabetes mellitus (T2DM) patients with carotid atherosclerosis. Patients with T2DM were divided into non-carotid atherosclerosis and carotid atherosclerosis groups, which were then subsequently divided into TT and TG + GG groups according to the adiponectin SNP45 T/G genotypes. Enzyme-linked immunosorbent assay, TaqMan probe quantitative polymerase chain reaction (PCR), PCR-TaqMan, color Doppler and other methods were used to determine the adiponectin levels, gene polymorphisms, acquired mitochondrial DNA (mtDNA) A3243G somatic cell mutation rates and the carotid intima-media thickness. The somatic cell mutation rate of acquired mtDNA A3243A/G in the T2DM carotid atherosclerosis group was significantly higher compared with the group without carotid atherosclerosis. In addition, the acquired mtDNA A3243A/G somatic cell mutation rate in the T2DM carotid atherosclerosis group with the adiponectin gene SNP45 TT genotype was significantly lower compared with the SNP45 TG/GG genotype group. T2DM combined with carotid atherosclerosis was associated with long-term oxidative stress. In addition, adiponectin gene SNP45 T/G was associated with increased mtDNA A3243A/G somatic mutation rates in T2DM patients with carotid atherosclerosis. Therefore, adiponectin gene polymorphisms may lead to diabetes atherosclerosis through oxidative stress.
Highlights
The morbidity of type 2 diabetes patients developing cardio vascular disease is 2-4 times as compared to people without diabetes
Out of the T2DM patients with carotid artery intima‐media thickness (IMT) thickening, 35% of them are due to causes of atherosclerosis that are already known and 65% of them are due to gene polymorphisms, oxidative stress and some other factors
The results of the present study revealed that significant differences existed in the mitochondrial DNA (mtDNA) A3243A/G somatic cell mutation rates between the NGT and T2DM groups (P
Summary
The morbidity of type 2 diabetes patients developing cardio vascular disease is 2-4 times as compared to people without diabetes. Out of the T2DM patients with carotid artery IMT thickening, 35% of them are due to causes of atherosclerosis that are already known and 65% of them are due to gene polymorphisms, oxidative stress and some other factors. A hyperglycemic state in diabetic patients causes the occurrence and development of atherosclerosis through oxidative stress. Oxidative stress hyperfunction in diabetic patients is four times higher than in individuals without the disease. The somatic mutation rate of acquired mitochondrial DNA (mtDNA) A3243G may be determined by TaqMan probe quantitative polymerase chain reaction (PCR) and this reflects the long‐term levels of oxidative stress in patients with T2DM [1,2]
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