Low normal free T4 confers decreased high-density lipoprotein antioxidative functionality in the context of hyperglycaemia

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Low normal thyroid function may promote the development of atherosclerotic cardiovascular disease by thus far poorly defined mechanisms. We tested the impact of thyroid function on HDL antioxidative capacity, a metric of its antiatherogenic functionality, in euthyroid subjects with varying degrees of glucose tolerance.

Design and Subjects

Seventy subjects with Type 2 diabetes mellitus (T2DM), 37 subjects with impaired fasting glucose (IFG) and 31 subjects with normal fasting glucose (NFG) (revised NCEP-ATPIII criteria) participated in a cross-sectional study.


HDL antioxidative capacity (standardized for HDL cholesterol) was measured as the percentage inhibition of low-density lipoprotein oxidation in vitro.


TSH, free T4 and HDL antioxidative capacity were not different among NFG, IFG and T2DM subjects (P > 0·25 for each). HDL antioxidative capacity was correlated positively with free T4 (r = 0·320, P = 0·007), and negatively with plasma glucose (r = −0·394, P < 0·001) in T2DM only. Taking account of age and sex, the relationship of HDL antioxidative functionality with free T4 was modified by glucose tolerance status (P = 0·040 and P = 0·008 for interactions of IFG and T2DM with free T4 respectively). Prevailing plasma glucose also interacted positively with free T4 on HDL antioxidative capacity (P = 0·054).


In the context of chronic hyperglycaemia, low free T4 within the euthyroid range confers diminished HDL antioxidative capacity, a pathophysiologically relevant metric of HDL functionality.

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