Nitric Oxide Gene Polymorphism is a Risk Factor for Diabetic Nephropathy and Atherosclerosis in Type 1 Diabetic Patients

AIM: To assess the risk factor for diabetic atherosclerosis nephropathy and diabetic nephropathy in type 1 diabetic patients. PATIENTS AND METHODS: Thirty healthy volunteers age and sex-matched and Sixty-five type 1 diabetic patient were in rolled in the study. The mean age of patients was 17.99 ± 2.59 years, mean age of onset of diabetes was 7.00 ± 3.28 years, mean duration of diabetes was 10.91 ± 3.54 years. Glycosylated sex-matched (HbA1c) was assessed in blood samples, serum lipid profile was determined, and serum level of oxidised low-density lipoprotein (OxLDL), and nitric oxide was evaluated by enzyme-linked immunosorbent assay (ELISA) technique. Nitric oxide 894G > T genotype was analysed by (PCR-RFLP) method and confirmed by Sequencing. Assessment of the albumin / creatinine ratio was done in urine samples. Renal Doppler and Carotid intima-media thickness (cIMT) via ultrasound was also performed. RESULTS: OxLDL, lipid profile, albumin/creatinine ratio, cIMT and resistivity index were significantly higher in diabetic patients while nitric oxide was significantly lower. Nitric oxide genotype shows no significant difference between diabetic’s patients and controls. Diabetic patients with homozygous NO had a significantly lower serum level of Nitric oxide, a significantly higher OxLDL, albumin / creatinine ratio and lipid profile. CONCLUSION: diabetic patients are liable for the occurrence of early diabetic nephropathy and atherosclerosis as a result of the presence of low level of nitric oxide. Nitric oxide gene polymorphism 894G > T in diabetic patients is a risk factor for diabetic nephropathy and atherosclerosis

Apelin, Nitric Oxide and Vascular Affection in Adolescent Type 1 Diabetic Patients

AIM: To evaluate the relationship of apelin and nitric oxide (NO) to endothelial dysfunction in type 1 diabetics. PATIENTS AND METHODS: Sixty two type 1 diabetics and 30 healthy age and sex matched controls were included. Blood samples for apelin, NO, glycosylated hemoglobin (HbA1c), and lipid profile were collected. Albumin/creatinine ratio was assessed in urine. Flow mediated dilatation (FMD) via ultrasound was done. RESULTS: The mean age of diabetics were 16.3 ± 1.5 yrs (14.0 – 19.0 yrs), and duration of disease, were 9.4 ± 2.9 yrs (5.0 – 16.5 yrs). FMD and FMD/nitrate mediated dilatation (NMD) ratio were lower in diabetics. NO was decreased, while apelin and albumin/creatinine ratio were increased significantly in diabetics. There was a positive correlation between apelin and HbA1c. On the contrary, NO had a negative correlation with HbA1c, albumin/creatinine ratio, LDL-c and OxLDL. CONCLUSION: Diabetic patients had endothelial dysfunction and high apelin level, with no related to each other. High level of apelin is associated with bad glycemic control. Obesity had no role to increase in apelin level. NO is related to diabetic nephropathy and atherosclerosis. We recommend a further large study to evaluate the relationship of apelin with endothelial dysfunction