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Osteoporosis

Effects of Sigma Anti-bonding Molecule Calcium Carbonate on bone turnover and calcium balance in ovariectomized rats

By | Osteoporosis

Effects of Sigma Anti-bonding Molecule Calcium Carbonate on bone turnover and calcium balance in ovariectomized rats

So-Young Choi, Dongsun Park, Goeun Yang, Sun Hee Lee, Dae Kwon Bae, Seock-Yeon Hwang, Paul K Lee, Yun-Bae Kim, Ill-Hwa Kim, Hyun-Gu Kang

This study was conducted to evaluate the effect of Sigma Anti-bonding Molecule Calcium Carbonate (SAC) as therapy for ovariectomy-induced osteoporosis in rats. Three weeks after surgery, fifteen ovariectomized Sprague-Dawley rats were divided randomly into 3 groups: sham-operated group (sham), ovariectomized group (OVX) and SAC-treatment group (OVX+SAC). The OVX+SAC group was given drinking water containing 0.0012% SAC for 12 weeks. Bone breaking force and mineralization as well as blood parameters related to the bone metabolism were analyzed. In OVX animals, blood concentration of 17β- estradiol decreased significantly, while osteocalcin and type I collagen C-terminal telopeptides (CTx) increased. Breaking force, bone mineral density (BMD), calcium and phosphorus in femurs, as well as uterine and vaginal weights, decreased significantly following OVX. However, SAC treatment (0.0012% in drinking water) not only remarkably restored the decreased 17β-estradiol and increased osteocalcin and CTx concentrations, but also recovered decreased femoral breaking force, BMD, calcium and phosphorus, although it did not reversed reproductive organ weights. It is suggested that SAC effectively improve bone density by preventing bone turnover mediated osteocalcin, CTx and minerals, and that it could be a potential candidate for therapy or prevention of menopausal osteoporosis.

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Role of the calcium-sensing receptor in parathyroid gland physiology

By | Osteoporosis

Role of the calcium-sensing receptor in parathyroid gland physiology

Randolph A. Chen and William G. Goodman

The calcium-sensing receptor (CaSR) represents the molecular mechanism by which parathyroid cells detect changes in blood ionized calcium concentration and modulate parathyroid hormone (PTH) secretion to maintain serum calcium levels within a narrow physiological range. Much has been learned in recent years about the diversity of signal transduction through the CaSR and the various factors that affect receptor expression. Beyond its classic role as a determinant of calcium-regulated PTH secretion, signaling through the CaSR also influences both gene transcription and cell proliferation in parathyroid cells. The CaSR thus serves a broad physiological role by integrating several distinct aspects of parathyroid gland function. The current review summarizes recent developments that enhance our understanding of the CaSR and its fundamental importance in parathyroid gland physiology.

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High-Dose Vitamin D and Calcium Attenuates Bone Loss with Antiretroviral Therapy Initiation: A Prospective, Randomized Placebo-Controlled Trial for Bone Health in HIV-Infected Individuals

By | Osteoporosis

High-Dose Vitamin D and Calcium Attenuates Bone Loss with Antiretroviral Therapy Initiation: A Prospective, Randomized Placebo-Controlled Trial for Bone Health in HIV-Infected Individuals

Edgar Turner Overton, MD, Ellen S. Chan, MSc, Todd T. Brown, MD, PhD, Pablo Tebas, MD, Grace A. McComsey, MD, Kathleen M. Melbourne, PharmD, Andrew Napoli, PhD, William Royce Hardin, BS, Heather J. Ribaudo, PhD, and Michael T. Yin, MD MS

Antiretroviral therapy (ART) has transformed HIV infection from a terminal disease to a manageable chronic illness. While incidence of AIDS-defining conditions has declined, other comorbidities have increased (1), including osteoporosis and fragility fractures (2-7). Both viral and host factors likely contribute to bone loss and fracture risk: HIV infection mediated by certain viral proteins, HIV-associated inflammation, lifestyle and behavioral factors, underlying genetic predisposition, comorbidities, and ART (8-14).

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Calcium Signalling and Calcium Transport in Bone Disease

By | Osteoporosis

Calcium Signalling and Calcium Transport in Bone Disease

H.C. Blair, P.H. Schlesinger, Christopher L.-H. Huang, and M. Zaidi

Calcium transport and calcium signalling mechanisms in bone cells have, in many cases, been discovered by study of diseases with disordered bone metabolism. Calcium matrix deposition is driven primarily by phosphate production, and disorders in bone deposition include abnormalities in membrane phosphate transport such as in chondrocalcinosis, and defects in phosphate-producing enzymes such as in hypophosphatasia. Matrix removal is driven by acidification, which dissolves the mineral. Disorders in calcium removal from bone matrix by osteoclasts cause osteopetrosis. On the other hand, although bone is central to management of extracellular calcium, bone is not a major calcium sensing organ, although calcium sensing proteins are expressed in both osteoblasts and osteoclasts. Intracellular calcium signals are involved in secondary control including cellular motility and survival, but the relationship of these findings to specific diseases is not clear. Intracellular calcium signals may regulate the balance of cell survival versus proliferation or anabolic functional response as part of signalling cascades that integrate the response to primary signals via cell stretch, estrogen, tyrosine kinase, and tumor necrosis factor receptors

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