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23-02-2006 | Thyroid | Article

Adipokines may mediate metabolic effects of thyroid disease

Abstract

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Study findings have indicated that the influence of thyroid disease on metabolism may be due to the effects of thyroid hormones on adipokines.

As many of the effects of thyroid abnormalities on the body are known to be associated with alterations in glucose and insulin metabolism, as well as changes in adipose tissue, the study authors decided to assess the relationship between thyroid abnormalities and adipokine hormones.

To this end, Katherine Cianflone, from the Université Laval in Québec, Canada, and co-workers examined levels of three adipokines - adiponectin, plasma acylation stimulating protein (ASP), and it's precursor, complement 3 (C3) - in 46 hyperthyroid patients, 23 hypothyroid individuals, and 30 healthy euthyroid controls.

They found that hyperthyroid participants had 95% more adiponectin, 47% less C3, but similar levels of ASP, and a higher ratio of ASP to C3, compared with control individuals.

Conversely, hypothyroid individuals demonstrated a 31% increase in ASP levels compared with control individuals.

Furthermore, in all participants, changes in each adipokine were associated with specific metabolic alterations. For example, in all participants, adiponectin levels were negatively correlated with body mass index (BMI), total cholesterol, and plasma triglyceride levels, while C3 was positively related to BMI and total cholesterol levels.

Of interest, individuals with high adiponectin levels were more likely to have high insulin and high-density lipoprotein cholesterol (HDL-C) levels than those without, whereas those with high C3 levels were less likely than those without to have elevated glucose, insulin, or HDL-C levels.

"In hyperthyroid subjects, adiponectin is increased in a state where there is increased fatty acid oxidation, whereas in hypothyroidism ASP is increased in a state where there is a push toward energy storage," Cianflone et al summarize.

"These changes suggest that thyroid disease may be accompanied by changes in adipokines, which may contribute to the phenotype expressed," they conclude.

This research was published in the journal Nutrition and Metabolism.