Too little blood-borne adiponectin may boost risk of thyroid cancer

Research conducted by a team of Greek and American endocrinologists has revealed that too little of the metabolic protein adiponectin in the blood may increase the likelihood of thyroid cancer, while higher levels may entail a lower-than-average risk of the disease.

Published ahead of print in the online version of the Journal of Clinical Endocrinology and Metabolism (JCEM), the study seems to confirm what has already been established for several other forms of carcinoma - namely, the inverse relationship between adiponectin and cancer risk.

The investigation was a result of collaboration between scientists at Boston's Beth Israel Deaconess Medical Center and pathologists from Greece's University of Athens and the Thessaloniki Theagenio Cancer Hospital.

From the start, the team focused on the relationship between circulating adiponectin levels and cancers of the thyroid.

They began by recruiting 175 thyroid cancer patients and 107 health control subjects. Researchers collected blood samples from all participants and tested them for levels of adiponectin.

According to a study published in the European Journal of Endocrinology, this protein helps the body control a number of metabolic processes, including blood sugar regulation and the breakdown of fatty acids.

The paper noted that higher levels of adiponectin are associated with increased insulin sensitivity, while lower levels are typically linked with increased triglycerides, body fat percentage and body mass index. However, prior to the latest JCEM report, its role in thyroid cancer risk had not be explored.

In the new study, endocrinologists found that thyroid cancer patients had, on average, a 12 percent lower adiponectin blood count than healthy volunteers.

The association between thyroid cancer risk and blood-borne levels of the protein was quite clear, the team wrote. Participants who fell within the highest quintile of adiponectin levels displayed just one-third the risk of developing any type of thyroid carcinoma, compared to those in the other quintiles.

The team did not stop there. Like several prior investigations into the relationship between adiponectin and cancer growth, scientists then extracted thyroid carcinoma samples from participants in order to measure the effect of adding more of the protein to the cellular environment.

In all, the group exposed 40 cell samples (mainly papillary and follicular, but including one sample each of medullary and anaplastic thyroid cancer) to recombinant adiponectin in test tubes.

The result?

"Recombinant adiponectin did not exert a clinically significant direct effect on cell cycle, proliferation, or apoptosis in thyroid cancer cell lines in vitro," the authors wrote. They added that while the relationship between the protein and the disease is inverse, it is almost certainly independent.

This means that adiponectin levels and thyroid cancer risk either hinge on a separate, third factor or are causally but indirectly linked. The team settled on the latter hypothesis.

"In the absence of a major direct effect of adiponectin on thyroid cancer cell lines, the negative association observed herein may be attributed to the metabolic effects of adiponectin," the researchers concluded.

The study is the latest in a spate of recent investigations into what link, if any, exists between adiponectin levels and cancer risk. 
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