Background: Nesfatin-1, a polypeptide encoded in the N-terminal region of the protein precursor Nucleobindin2 (NUCB2), functions in the regulation of fat storage and hunger. Nesfatin-1 co-localizes with thyrotropin-releasing hormone (TRH) and has a role in affecting the membrane potential of TRH neurons in the posteroventral nucleus (PVN). Data about nesfatin-1 levels in thyroid dysfunction is limited and controversial.
Objective: This current study aimed to evaluate serum nesfatin-1 levels in the euthyroid, hypothyroid, and hyperthyroid rats.
Materials and methods: Forty two adult male albino western mature rats were divided into three equal main groups: Group I (Euthyroid) was used as control group,Group II (Hypothyroid) were treated with propylthiouracil for 4 weeks, and Group III (Hyperthyroid) were treated with eltroxin for 4 weeks. In all groups, serum glucose, insulin, nesfatin-1, T3, T4, TSH and lipid profile were assayed.
Results: In hyperthyroid group compared to control group, there were significant rise in serum levels of nesfatin-1, T3, T4, insulin, glucose, HDL and level of HOMA-IR and a significant decrease in serum level of TSH l. However, there was a non-significant change in serum level of nesfatin-1 in hypothyroid group compared to control group. Furthermore, there were significant elevations in serum level of TSH, TC, TG and LDL and significant decreases in serum level of T3, T4 and HDL in hypothyroid group. There was a significant positive correlation between serum nesfatin-1 levels with T3, T4, serum levels of insulin, glucose, HOMA IR and HDL and significant negative correlations between serum nesfatin-1 levels with serum TSH, LDL levels, food intake and BMI in hyperthyroid group. However, there were significant positive correlations between serum nesfatin-1 level with T3, and HDL, and a significant negative correlation between serum nesfatin-1 level with food intake in hyporthyroid group.
Conclusion: Hyperthyroid state was accompanied by increased nesfatin-1 level, while hypothyroid state did not influence the nesfatin-1 level.