Thyroid status influence on adiponectin, acylation stimulating protein (ASP) and complement C3 in hyperthyroid and...

Area of Science:

• Endocrinology and Metabolism Research
• Adipokine Signaling Pathways
• Thyroid Hormone Physiology

Background:

• Thyroid dysfunction (hyperthyroidism, hypothyroidism) significantly impacts intermediary metabolism, affecting body weight, insulin resistance, and lipid profiles.
• Adipokines, such as adiponectin and acylation stimulating protein (ASP), play crucial roles in metabolic regulation.
• Understanding the interplay between thyroid status and adipokines is essential for comprehending metabolic disturbances in thyroid disease.

Purpose of the Study:

• To investigate plasma levels of adiponectin, its precursor complement C3, and acylation stimulating protein (ASP) in individuals with hyperthyroidism and hypothyroidism compared to healthy controls.
• To explore the correlations between these adipokines and thyroid hormones (FT3, FT4, TSH), metabolic parameters (glucose, insulin, lipids, BMI), and insulin resistance markers (HOMA-IR).

Main Methods:

• Recruitment of 99 subjects: 46 hyperthyroid, 23 hypothyroid, and 30 control subjects from endocrinology clinics.
• Comprehensive evaluation including thyroid function tests (FT4, FT3, TSH), glucose, insulin, lipid profiles, and adipokines (adiponectin, ASP, C3).
• Statistical analysis to compare groups and assess correlations between adipokines, thyroid hormones, and metabolic markers.

Main Results:

• Hyperthyroidism was linked to a significant increase in adiponectin (95%) and an elevated ASP/C3 ratio, with no change in ASP. Hypothyroidism showed a 31% increase in ASP.
• Adiponectin and C3 levels correlated with FT3 and FT4. ASP correlated with TSH. ASP and C3 showed a negative correlation.
• Adiponectin negatively correlated with BMI, total cholesterol, and triglycerides. C3 positively correlated with BMI and total cholesterol. Adiponectin positively correlated with insulin and HOMA-IR, while C3 showed negative correlations with glucose, insulin, and HOMA-IR.

Conclusions:

• Thyroid disease is associated with significant alterations in adipokine profiles, including adiponectin, ASP, and C3.
• These adipokine changes may contribute to the metabolic phenotype observed in hyperthyroid and hypothyroid individuals.
• Further research is warranted to elucidate the specific mechanisms by which thyroid hormones influence adipokine expression and function.