The thyroid gland has an important role in determining how much energy the body burns. Thyroid gland functions are regulated by a hormone known as thyroid-stimulating hormone (TSH). Increased levels of TSH, as well as increased signaling through the receptor for TSH, result in hyperthyroidism (characterized by weight loss because the body increases the amount of energy it burns) and goiter.
Signals downstream of the receptor for TSH had been thought to be mediated mainly by a protein complex known as Gs. But now, a study that appears online on August 9, in advance of publication in the September print issue of the Journal of Clinical Investigation, indicates that in mice Gq/G11-mediated signaling has an essential role in transmitting TSH-induced signals and therefore in regulating thyroid gland function. This makes Gq and G11 potential new targets for the treatment of hyperthyroidism and goiter.
In the study, Stefan Offermanns and colleagues from the University of Heidelberg, Germany, generated mice lacking the alpha-subunits of both Gq and G11 only in cells of the thyroid gland. These mice had reduced thyroid gland function and many had symptoms similar to individuals with hypothyroidism. In addition, the thyroid gland in these mice was unresponsive to the proliferative effects of TSH and a goitrogenic diet.
The authors therefore suggest that inhibiting Gq and G11, or the molecules activated downstream of these G proteins, might be of therapeutic benefit for individuals with diseases characterized by increased thyroid gland function and/or growth.
Article: Thyrocyte-specific Gq/G11 deficiency impairs thyroid function and prevents goiter development
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
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