Investigation of serum adropin level in patients with subclinic hypothyroid

Introduction and Aim: Thyroid hormones secreted from the thyroid gland are hormones that have a regulating effect on the growth and development of all body cells and energy metabolism. Subclinical hypothyroidism is a condition in which thyroxine (fT4) and triiodothyronine (fT3) levels are within the reference ranges, as well as increased serum thyroid stimulating hormone (TSH) concentration. Subclinical hypothyroidism, which may be a precursor to hypothyroidism; It can be effective especially in the development of metabolic syndrome, insulin resistance, cardiovascular system diseases, endothelial dysfunction and atherosclerosis. Adropin is a peptide hormone primarily encoded by the gene (Enho) associated with energy homeostasis in the liver and brain. It is closely related to glucose and lipid homeostasis balance and insulin resistance. It is produced in many tissues and organs such as the liver, brain, heart, kidney, pancreas and gastrointestinal tract. The aim of our study; we aimed to determine whether adropin level changes in SCH patients and thus to determine whether it will be a mediator marker in the clinical outcomes and pathophysiology of subclinical hypothyroidism. Materials and Methods: Volunteers without a history of acute or chronic disease and any drug use, including antithyroid drugs, were included in the study. Individuals were divided into 2 groups according to their TSH level as subclinical hypothyroidism (TSH: 5-10 mIU/l ) (n:41) and euthyroid control (n:43). Biochemical parameters, thyroid function tests, serum adropin levels of all volunteers were studied and the results were compared statistically. Results: There was no statistically significant difference between the groups in terms of age, gender and body mass index (BMI) (p >0.05). Between the two groups, the adropin level was 136.75± 41.87 ng/ml in the SCH group; In the control group, it was determined as 220.65± 64.93 ng/ml and a statistically significant difference was found between the groups according to the serum adropin level (p<0.001). While a negative correlation was found between adropin level and TSH (r:-0.765; p:<0.001); No significant correlation was found with FT3 and FT4 (r: -0.033; p: 0.765, r: 0.075; p:0.496, respectively). Conclusion: Serum adropin level was found to be significantly lower in SCH patients compared to controls. We think that this is due to the fact that the tissues in which adropin synthesis is made affect the ENHO gene expression through direct or indirect mechanisms with the pathophysiological or metabolic events that develop with the thyroid hormone level. More work is needed to elucidate these possible mechanisms. Keywords: Adropin, subclinical hypothyroidism, metabolic syndrome, insulin resistance, atherosclerosis