Associations between cardiovascular risk, insulin resistance, β-cell function and thyroid dysfunction: a cross-sectional study in She ethnic minority group of Fujian Province in China

Author:

Chen Gang,Wu Juan,Lin Yinghua,Huang Baoying,Yao Jin,Jiang Qiqin,Wen Junping,Lin Lixiang

Abstract

ObjectiveTo investigate the associations between cardiovascular risk, insulin resistance (IR), β-cell function and thyroid dysfunction in She ethnic minority group in China.MethodsWe enrolled 5080 participants of She ethnicity in this analysis eventually. We measured serum TSH and thyroid peroxidase antibody (TPOAb) concentrations, blood glucose and insulin levels in both fasting and 2-h postprandial states, serum lipid levels, blood pressure (BP), brachial–ankle pulse wave velocity (baPWV), electrophysiological parameters, includingTpeakTendinterval (Tp–e), QT interval and height of the R wave in lead aVL (RaVL), and anthropometric parameters.ResultsThe total prevalence of thyroid dysfunction in this population is 12.1%. Hyperthyroid subjects had shorterTp–einterval and QT interval in electrocardiogram (ECG), while hypothyroid subjects had shorterTp–einterval and longer QT interval in ECG than euthyroid subjects. Neither hyperthyroid nor hypothyroid subjects showed significant difference in BP, pulse pressure, and baPWV compared with euthyroid subjects. RaVL was slightly higher in hyperthyroid subjects, though the difference did not reach statistical significance (P=0.08). Subjects with TSH<0.3 mIU/l had higher blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), and β-cell function (HOMA-β), whereas subjects with TSH>10 mIU/l had lower insulin, HOMA-IR, and HOMA-β than the reference group. There was a significant negative correlation, albeit weak, between TSH and HOMA-IR, HOMA-β after adjustment for confounding factors.ConclusionsHypothyroid subjects may carry higher cardiovascular risk than euthyroid subjects. Moreover, IR and β-cell function are inversely correlated with TSH, which may be explained by the decreasing insulin-antagonistic effects of thyroid hormones along with increasing TSH.

Publisher

Bioscientifica

Subject

Endocrinology,General Medicine,Endocrinology, Diabetes and Metabolism

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