Obesity has recently been mentioned as a metabolic pandemic in developed and developing countries and is an important known risk factor for type 2 diabetes and cardiovascular diseases. The main mechanism responsible for obesity is insulin resistance. Adropin is a peptide-structured regulatory hormone that is suggested to play a role in insulin resistance and metabolic regulation. We aimed to evaluate the associations of serum adropin with insulin resistance and clarify the factors affecting serum adropin concentrations. The study included 50 obese patients and 22 healthy controls. Patients with chronic disease and drug use history were excluded. Serum adropin and other metabolic parameters were obtained after overnight fasting. ELISA was used to measure serum adropin concentrations. The homeostatic model assessment-insulin resistance (HOMA-IR) index was used to calculate insulin resistance. Insulin resistance was defined as HOMA-IR >2.5. Serum adropin values were found to be low in the obese otherwise healthy patient group (p<0.001). Linear regression analysis revealed that age, body mass index (BMI), waist circumference (WC), high-density lipoprotein cholesterol, fasting glucose, and HOMA-IR affect serum adropin level. In multiple regression analysis, age is the most significant factor affecting serum adropin concentration. Serum adropin concentrations were negatively correlated with BMI, WC, diastolic blood pressure, fasting glucose, and insulin. Serum adropin concentrations were low in obese patients and the optimum cut-off point for adropin to indicate HOMA-IR at 2.5 is 216.7 ng/L. The findings suggest that serum adropin may contribute to the regulation of glycolipid metabolism and insulin resistance in obese patients.
Data availability statement
All data relevant to the study are included in the article or uploaded as supplementary information. Data are available upon request to email@example.com.
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Contributors Study concept and design: HE, AO. Analysis and interpretation of data: MES, BB. Drafting of the manuscript: HE, SIC.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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