Thyroid gland disorders are among the most common endocrine abnormalities encountered by physicians. Changes in weight, body temperature and fat tissue occur in patients with thyroid dysfunction. Thyroid hormones affect or are affected by body weight, body fat mass, body temperature, insulin resistance, glucose and lipid metabolism [1].
Subclinical Hypothyroidism (SH) is the most common thyroid dysfunction [2].
This condition is mentioned if serum TSH levels are more than 4 mIU/L but fT3 and fT4 levels are within the reference value [3, 4]. The prevalence of SH varies between 4–10% depending on age and gender. The incidence of this disease increases with age [5]. It is twice as common in women as in men [6]. While the most common cause of SH is iodine deficiency, in cases where there is sufficient external iodine intake, Hashimoto's thyroiditis, thyroid surgery, thyroid ablation treatment, radiotherapy treatment and medications (lithium, amiodarone) stand out as the underlying cause [7].
Subclinical Hypothyroidism is evaluated in two groups: mild SH (if TSH levels are between 4 and 10 mIU/L), and severe SH( if TSH levels are > 10 mIU/L[8]. In subclinical hypothyroidism patients, symptoms may often be absent. However, some potential consequences of subclinical hypothyroidism include cardiac dysfunction [9], atherosclerotic disease [10], an increase in LDL cholesterol [11], systemic hypothyroid symptoms[12], neuropsychiatric symptoms [13], and progression to symptomatic hypothyroidism[14, 15].
Chemerin protein is a recently discovered as adipokine released from adipose tissue, and research on it is steadily increasing. Exactly, it binds with G-protein to form a ligand for the CMKLR1 receptor, also known as Chem R23 or GPCR-DEZ. It has been found that chemerin is expressed in many organs with metabolic effects, such as adipose tissue, liver, kidney, pancreas, lungs, ovaries, pituitary gland, etc.[16]. Chemerin synthesized from adipose tissue has both autocrine and paracrine effects. The autocrine response of chemerin involves being associated with lipolysis, glucose uptake, and metabolic pathways. Its paracrine response is related to chronic low-level inflammation associated with obesity [17]. Chemerin's CMKLR1 receptor is found on neutrophils, activated macrophages, dendritic cells, and was initially identified as a chemotactic protein. Chemerin is now clearly associated with adipogenesis, osteoclastogenesis, angiogenesis, Metabolic Syndrome (MetS), Type 2 diabetes, arthritis, and Crohn's disease [18].
Sfrp5 is a member of the Sfrp family produced from adipose tissue and is a novel adipokine with anti-inflammatory properties that has beneficial effects on metabolic functions. Initially, it was found to be expressed in retinal pigment epithelial cells and the pancreas[19]. It was found that Sfrp5 is highly present in white adipose tissue, especially visceral adipose tissue [20]. In healthy individuals, Sfrp5 exerts an anti-inflammatory effect by suppressing Wnt signaling via Wnt5a. In obese individuals, this balance is disrupted, and the WNT5a/Sfrp5 protein expression ratio increases [21]. Exacerbation of metabolic dysfunction caused by Sfrp5 deficiency is associated with macrophage accumulation in adipose tissues and increased production of pro-inflammatory cytokines, including TNF and IL-6, whereas overexpression of Sfrp5 causes inhibition of JUN N-terminal kinase 1, a target of non-canonical Wnt signaling, in adipocytes. It has been shown to inhibit phosphorylation and block the production of pro-inflammatory cytokines by macrophages [22, 23].
For these reasons, the relationship between adipokine release and thyroid dysfunction has attracted the attention of researchers. So in this study we aimed to evaluate the relationship between clinical and biochemical parameters of SH and serum chemerin and Sfrp5 levels.