The parathyroid is a target organ for FGF23 in rats

The parathyroid is a target organ for FGF23 in rats

December 2007 | Iddo Z. Ben-Dov, Hillel Galitzer, Vardit Lavi-Moshayoff, Regina Goetz, Makoto Kuro-o, Moosa Mohammadi, Roy Sirkis, Tally Naveh-Many, and Justin Silver
The study investigates the role of FGF23 in the parathyroid gland of rats. FGF23, a bone-derived hormone that regulates phosphate homeostasis, acts through FGF receptors (FGFRs) and the coreceptor Klotho. The researchers found that the parathyroid gland expresses Klotho and FGFRs, and that administration of recombinant FGF23 increased Klotho levels and activated the MAPK pathway in the parathyroid. FGF23 also suppressed parathyroid hormone (PTH) secretion and PTH gene expression in both rats and in vitro cultures. The decrease in PTH secretion was prevented by a MAPK inhibitor, indicating that FGF23 acts directly on the parathyroid through the MAPK pathway to reduce serum PTH levels. This discovery adds a new dimension to the understanding of mineral homeostasis by highlighting the bone-parathyroid endocrine axis.The study investigates the role of FGF23 in the parathyroid gland of rats. FGF23, a bone-derived hormone that regulates phosphate homeostasis, acts through FGF receptors (FGFRs) and the coreceptor Klotho. The researchers found that the parathyroid gland expresses Klotho and FGFRs, and that administration of recombinant FGF23 increased Klotho levels and activated the MAPK pathway in the parathyroid. FGF23 also suppressed parathyroid hormone (PTH) secretion and PTH gene expression in both rats and in vitro cultures. The decrease in PTH secretion was prevented by a MAPK inhibitor, indicating that FGF23 acts directly on the parathyroid through the MAPK pathway to reduce serum PTH levels. This discovery adds a new dimension to the understanding of mineral homeostasis by highlighting the bone-parathyroid endocrine axis.
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