Rat model of the hypercalcaemia induced by parathyroid hormone-related protein: characteristics of three bisphosphonates

Komatsu, Yoshimitsu; Imai, Yohsuke; Itoh, Fumiaki; Kojima, Masami; Isaji, Masayuki; Shibata, Nobuhiko

doi:10.1016/j.ejphar.2004.11.050

Cited by 4 publications

(5 citation statements)

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“…Hypercalcemia and dehydration are related to reduced renal function [34,35]. We thought to determine how hypercalcemia and dehydration occur in mdx mice and the relationship between those symptoms and renal function.…”

Section: Discussionmentioning

confidence: 99%

Renal involvement in the pathogenesis of mineral and bone disorder in dystrophin-deficient mdx mouse

et al. 2019

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Duchenne muscular dystrophy is a severe muscular disorder, often complicated with osteoporosis, and impaired renal function has recently been featured. We aimed to clarify the involvement of renal function in the pathogenesis of mineral and bone disorder in mdx mice, a murine model of the disease. We clearly revealed renal dysfunction in adult mdx mice, in which dehydration and hypercalcemia were contributed. We also examined the effects of dietary phosphorus (P) overload on phosphate metabolism. Serum phosphate and parathyroid hormone (PTH) levels were significantly increased in mdx mice by dietary P in a dose-dependent manner; however, bone alkaline phosphatase levels were significantly lower in mdx mice. Additionally, bone mineral density in mdx mice were even worsened by increased dietary P in a dose-dependent manner. These results suggested that the uncoupling of bone formation and resorption was enhanced by skeletal resistance to PTH due to renal failure in mdx mice.

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Section: Discussionmentioning

confidence: 99%

Renal involvement in the pathogenesis of mineral and bone disorder in dystrophin-deficient mdx mouse

et al. 2019

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“…Additionally, while most models share in vivo features of the human syndrome, there are notable differences that must be considered. For example, rodent models with human or canine cancer xenografts and CAH consistently have high levels of serum calcitriol that contribute to CAH to varying degrees; however, humans with CAH usually have low serum calcitriol concentrations [ 45 , 86 , 87 ]. This review focuses on the comparative aspects of HHM and LOH in humans and animals, with a discussion of the available animal models for CAH research.…”

Section: Introductionmentioning

confidence: 99%

Animal Models of Cancer-Associated Hypercalcemia

Kohart

Elshafae

Breitbach

et al. 2017

Veterinary Sciences

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Cancer-associated hypercalcemia (CAH) is a frequently-occurring paraneoplastic syndrome that contributes to substantial patient morbidity and occurs in both humans and animals. Patients with CAH are often characterized by markedly elevated serum calcium concentrations that result in a range of clinical symptoms involving the nervous, gastrointestinal and urinary systems. CAH is caused by two principle mechanisms; humorally-mediated and/or through local osteolytic bone metastasis resulting in excessive calcium release from resorbed bone. Humoral hypercalcemia of malignancy (HHM) is the most common mechanism and is due to the production and release of tumor-associated cytokines and humoral factors, such as parathyroid hormone-related protein (PTHrP), that act at distant sites to increase serum calcium concentrations. Local osteolytic hypercalcemia (LOH) occurs when primary or metastatic bone tumors act locally by releasing factors that stimulate osteoclast activity and bone resorption. LOH is a less frequent cause of CAH and in some cases can induce hypercalcemia in concert with HHM. Rarely, ectopic production of parathyroid hormone has been described. PTHrP-mediated hypercalcemia is the most common mechanism of CAH in human and canine malignancies and is recognized in other domestic species. Spontaneous and experimentally-induced animal models have been developed to study the mechanisms of CAH. These models have been essential for the evaluation of novel approaches and adjuvant therapies to manage CAH. This review will highlight the comparative aspects of CAH in humans and animals with a discussion of the available animal models used to study the pathogenesis of this important clinical syndrome.

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“…Thus, elevated PTHrP in vivo causes hypercalcemia, anorexia, and nephrocalcinosis (18,19,23,37,47). In adulthood, PTHrP is not normally found circulating in the plasma (38).…”

Section: E460mentioning

confidence: 99%

“…Kidneys from euthanized animals were immediately placed in 3.8% formalin at 4°C overnight before embedding in paraffin for processing. Renal cortical slices were then deparrifinized with xylene and dehydrated with an ethanol gradient before staining for tissue calcification with von Kossa's stain, as described previously (23).…”

Section: Analysesmentioning

confidence: 99%

Parathyroid hormone-related protein stimulates plasma renin activity via its anorexic effects on sodium chloride intake

Atchison

Westrick

Szandzik

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Rat model of the hypercalcaemia induced by parathyroid hormone-related protein: characteristics of three bisphosphonates

Cited by 4 publications

References 32 publications

Renal involvement in the pathogenesis of mineral and bone disorder in dystrophin-deficient mdx mouse

Renal involvement in the pathogenesis of mineral and bone disorder in dystrophin-deficient mdx mouse

Animal Models of Cancer-Associated Hypercalcemia

Parathyroid hormone-related protein stimulates plasma renin activity via its anorexic effects on sodium chloride intake

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