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Adenomatous human parathyroid cells exhibit impaired sensitivity to L-amino acids
Journal of Clinical Endocrinology and Metabolism, 07/02/09

Conigrave AD et al. - Impaired L-amino acid sensing by calcium-sensing receptors in adenomatous parathyroid cells contributes to the loss of feedback control of PTH secretion in primary hyperparathyroidism. The CaR's amino acid binding site may be exploited as a target in the medical treatment of primary and perhaps other forms of hyperparathyroidism.

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A. D. Conigrave, 07/02/09

There are two prominent features of parathyroid adenomatous disease: impaired control of cell number and impaired feedback control of parathyroid hormone (PTH) secretion by calcium. The calcium-sensing receptor mediates the regulation of both and is expressed on the cell surface at reduced levels in parathyroid adenomas when compared with normal parathyroid tissue. Interestingly, receptor function is modulated not only by calcium but also other nutrients including notably L-amino acids, the building blocks of proteins. In this work, we show that amino acid sensing by the calcium-sensing receptor is impaired in adenomatous disease, resulting in a secondary impairment of calcium sensitivity. The work raises some important new questions: e.g., 1. What are the dietary protein requirements of normal parathyroid function? 2. Can the amino acid binding site on the receptor be exploited by either dietary or pharmacological means to restore gland function? The work also highlights a question that goes to the heart of the problem: What is the molecular basis for the loss of calcium-sensing receptor expression in parathyroid adenomas?

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