In several families it has been shown that children with an imbalance in their serum levels of thyroid hormones as well as neurological and mental deficits (psychomotor retardation) have a defect in their MCT8 gene. But why defects in MCT8 - which produces a protein that allows cells to take up thyroid hormones - cause these thyroid hormone defects and psychomotor retardation is not clear, in part, because there are few animal models of the disease. In a study that appears online in advance of publication in the March print issue of the Journal of Clinical Investigation, Heike Heuer and colleagues studied mice lacking MCT8 and found that they exhibited similar patterns of thyroid hormone imbalance to humans with an MCT8 gene defect. However, the mice did not develop neurological defects, leading the authors to suggest that mice, but not humans, have thyroid hormone transporters able to compensate for the lack of MCT8. Identifying these transporters is important for the development of a good mouse model of the psychomotor retardation caused by MCT8 gene defects in humans, something that is crucial for increasing our understanding of the human disease.
TITLE: Abnormal thyroid hormone metabolism in mice lacking the monocarboxylate transporter 8
AUTHOR CONTACT:
Heike Heuer
Leibniz Institute for Age Research/Fritz Lipmann Institute, Jena, Germany.
JCI table of contents -- February 22, 2006
Contact: Karen Honey
Journal of Clinical Investigation
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