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- W2302419673 abstract "Type 2 diabetes mellitus (T2DM) is a metabolic and chronic disease which is characterized by hyperglycemia, and that is the major causes of various micro and macrovascular complications. Asymmetrical dimethylarginine (ADMA), formed by the hydrolysis of proteins containing methylated arginine residues, is an endogenous inhibitor of nitric oxide synthase (NOS), which oxidize l-arginine to citruline and nitric oxide (NO), related to hyperinsulinaemia and hyperlipidaemia. Apelin is a recently discovered peptide, present in a number of tissues and play role in insulin sensitivity improvement. In this study, our aim was to determine the levels of apelin and ADMA with glycated haemoglobin (HbA1c) in type 2 diabetic patients with or without vascular complications. This study included (a total of) 59 diabetic patients. Of the patients, 30 were diabetic with complications, and 29 without complications. In serum samples obtained from the patients, serum ADMA and apelin levels were measured with Enzyme Linked Immunosorbent Assay (ELISA) method. Our study totally enrolled 59 patients in two groups. No significant differences were found in sex, age, HbA1c and glucose levels among groups. Apelin and ADMA levels of group with complications were lower than those of group without complications, but no statistically significant difference of apelin and ADMA levels (p > 0.05). The results of this study have been showed no statistically significant relationship present between ADMA–apelin levels and complications of T2DM. Further studies involving larger patients populations and healthy controls should be done to clarify the pathogenetic significance of apelin and ADMA in diabetic vascular complications." @default.
- W2302419673 created "2016-06-24" @default.
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- W2302419673 date "2016-04-01" @default.
- W2302419673 modified "2023-10-18" @default.
- W2302419673 title "Serum apelin and ADMA levels in type 2 diabetics with and without vascular complications" @default.
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- W2302419673 doi "https://doi.org/10.1016/j.dsx.2016.03.005" @default.
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