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

Author(s): Yu Haiying | Yang Yan | Zhang Muxun | Lu Huiling | Zhang Jianhua | Wang Hongwei | Cianflone Katherine

Journal: Nutrition & Metabolism
ISSN 1743-7075

Volume: 3;
Issue: 1;
Start page: 13;
Date: 2006;
Original page

Abstract Background Thyroid abnormalities (hyperthyroid and hypothyroid) are accompanied by changes in intermediary metabolism including alterations in body weight, insulin resistance and lipid profile. The aims of this study were to examine plasma ASP, its precursor C3 and adiponectin in hyperthyroid and hypothyroid subjects as compared to controls. Methods A total of 99 subjects were recruited from endocrinology/out-patient clinics: 46 hyperthyroid subjects, 23 hypothyroid subjects and 30 control subjects. Subjects were evaluated for FT4, FT3, TSH, glucose, insulin, complete lipid profile and the adipokines: adiponectin, acylation stimulating protein (ASP) and complement C3. Results Hyperthyroidism was associated with a 95% increase in adiponectin (p = 0.0002), a 47% decrease in C3 (p < 0.0001), no change in ASP and increased ASP/C3 ratio (p = 0.0012). Hypothyroidism was associated with a 31% increase in ASP (p = 0.008). Adiponectin and C3 correlated with FT3 (r = 0.383, p = 0.004 and r = -0.277, p = 0.007, respectively) and FT4 (r = 0.464, p = 0.003 and r = -0.225, p = 0.03, respectively). ASP correlated with TSH (r = 0.202, p = 0.04). Adiponectin did not correlate with either ASP or C3, only ASP and C3 correlated (r = -0.197, p = 0.05). Adiponectin was negatively correlated with BMI, total cholesterol and plasma triglyceride, while C3 was positively correlated with BMI and total cholesterol. Surprisingly, adiponectin was positively correlated with insulin (r = 0.293, p = 0.02) and HOMA-IR (r = 0.373, p = 0.003) while C3 was negatively correlated with glucose (r = -0.242, p = 0.022, insulin (r = -0.184, p = 0.05) and HOMA-IR. Conclusion These changes suggest that thyroid disease may be accompanied by changes in adipokines, which may contribute to the phenotype expressed.
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