Abstract
Ideal hypoparathyroidism animal models are a prerequisite to developing new treatment modalities for this disorder. The purpose of this study was to evaluate the feasibility of a model whereby rats were parathyroidectomized (PTX) using a fluorescent-identification method and the ideal calcium content of the diet was determined. Thirty male rats were divided into surgical sham (SHAM, n = 5) and PTX plus 0, 0.5, and 2% calcium diet groups (PTX-FC (n = 5), PTX-NC (n = 10), and PTX-HC (n = 10), respectively). Serum parathyroid hormone levels decreased to non-detectable levels in all PTX groups. All animals in the PTX—FC group died within 4 days after the operation. All animals survived when supplied calcium in the diet. However, serum calcium levels were higher in the PTX-HC than the SHAM group. The PTX-NC group demonstrated the most representative modeling of primary hypothyroidism. Serum calcium levels decreased and phosphorus levels increased, and bone volume was increased. All animals survived without further treatment and did not show nephrotoxicity including calcium deposits. These findings demonstrate that PTX animal models produced by using the fluorescent-identification method, and fed a 0.5% calcium diet, are appropriate for hypoparathyroidism treatment studies.
Highlights
Hypoparathyroidism is a state of parathyroid hormone (PTH) deficiency that is induced by many medical conditions
[9] We reported previously a surgically excised hypoparathyroidism animal model using the 5-animolevulinic acid (5-ALA) fluorescent-identification method
[20] the long-term observational animal experiment with female rat could be considered to evaluate the feasibility of the hypoparathyroidism animal model in future study. We suggest that this hypoparathyroidism animal model produced by parathyroidectomy is highly reproducible when using the fluorescent-identification method and the animals are fed the standard purified American Institute of Nutrition (AIN)-93G diet
Summary
Hypoparathyroidism is a state of parathyroid hormone (PTH) deficiency that is induced by many medical conditions. The most common etiology is accidental excision of the parathyroid gland during thyroid surgery. [1, 2] PTH increases phosphorus excretion by the kidney, stimulates calcium absorption by the renal tubules and small intestine, and activates osteoclasts to enhance bone turnover. PTH activates vitamin D in the kidney. PTH deficiency leads to a loss of calcium homeostasis and hypocalcemia. This condition causes neurophysiologic disturbances including paresthesia, weakness, irritability, and muscle cramping. This condition causes neurophysiologic disturbances including paresthesia, weakness, irritability, and muscle cramping. [2]
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