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"Calcium and Metabolic Bone Disorders"Dr. Andrew Karaplis (biography)
English - 2005-08-13 - 62 minutes
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Summary :
We are currently in the Bone and Joint Decade, and in this presentation Dr. Karaplis gives an overview of several research advances made recently in the field of bone metabolism.
In the last decade, the role of parathyroid hormone (PTH) in calcium homeostasis has come to be understood, and the PTH receptor has been identified in targets tissues such as bone and the renal tubule. Constitutively activating mutations in the PTH receptor have been found in patients with Jansen's metaphyseal chondrodysplasia (1), and inactivating mutations in the PTH receptor lead to another form of chondrodysplasia called Blomstrand's chondrodysplasia (2). Binding of calcium to the calcium sensing receptor primarily located in the parathyroid gland, leads to inhibition of PTH secretion. Inactivating and activating mutations in this receptor are also implicated in disease states.
Is there a phosphate regulating hormone? Dr. Karaplis presents studies suggesting that there is (3,4), and this could be important for bone diseases arising due to chronic renal failure.
The U.S National Institutes of Health 2002 definition of osteoporosis says that it is a skeletal disorder characterised by compromised bone strength, predisposing the person to an increased risk of fracture. Bone strength consists of bone density, and bone quality for which there is presently no means of clinical assessment. In the last few years, certain gene mutations have been found to affect bone density. A mutation in the LDL Receptor-Related Protein 5 (LRP5), for example, was found to cause high bone density (5). In another condition called sclerosteosis involving an overgrowth of normal bone, increased bone density was found to be due to a (SOST) protein deficiency (6). Dr. Karaplis reviews the therapeutic options for osteoporosis, and discusses findings from the Women's Health Initiative study relating to HRT and the incidence of hip fractures.
Lastly Dr. Karaplis talks about the paradox of PTH – if given continuously, it can cause bone breakdown and osteoporosis, but when given intermittently and in a pulsatile fashion, it promotes bone formation.
Copyright © 2005 E-MedHosting.com Inc.
Learning objectives :
After viewing this presentation the participant will be able to discuss recent developments in research on bone metabolism:
- Parathyroid hormone and calcium homeostasis
- Evidence for a phosphate regulating hormone
- Osteoporosis: definition and therapeutic options
- Gene mutations affecting bone density
Bibliographic references :
1. E. Schipani, M.D., Ph.D., C.B. Langman, M.D., A.M. Parfitt, M.D., G.S. Jensen, B.A., S. Kikuchi, M.D., S.W. Kooh, M.D., Ph.D., W.G. Cole, M.D., Ph.D., and H. Jüppner, M.D.Constitutively Activated Receptors for Parathyroid Hormone and Parathyroid Hormone–Related Peptide in Jansen's Metaphyseal Chondrodysplasia N Engl J Med. 1996 Sep 5;335(10):708-14.
2. Andrew C. Karaplis, Bin He, M. T. Audrey Nguyen, Ian D. Young, David Semeraro, Hidehiro Ozawa and Norio Amizuka Inactivating Mutation in the Human Parathyroid Hormone Receptor Type 1 Gene in Blomstrand Chondrodysplasia Endocrinology Vol. 139, No. 12 5255-5258.
3. F. Francis, S. Hennig, B. Korn, R. Reinhardt, P. de Jong, A. Poustka, H. Lehrach, P.S.N Rowe, J.N. Goulding, T. Summerfield, R. Mountford, A.P. Read, E. Popowska, E. Pronicka, K.E. Davies, J.L.H. O'Riordan, M.J. Econs, T. Nesbitt, M.K. Drezner, C. Oudet, S. Pannetier, A. Hanauer, T.M. Strom, A. Meindl, B. Lorenz, B. Cagnoli, K.L. Mohnike, J. Murken1 & T. MeitingerA gene (PEX) with homologies to endopeptidases is mutated in patients with X−linked hypophosphatemic rickets Nature Genetics 11, 130 - 136 (1995).
4. Kenneth E. White, Wayne E. Evans, Jeffery L.H. O'Riordan, Marcy C. Speer, Michael J. Econs, Bettina Lorenz-Depiereux, Monika Grabowski, Thomas Meitinger & Tim M. Strom. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23 Nature Genetics 26, 345 - 348 (2000).
5. Lynn M. Boyden, Ph.D., Junhao Mao, Ph.D., Joseph Belsky, M.D., Lyle Mitzner, M.D., Anita Farhi, R.N., Mary A. Mitnick, Ph.D., Dianqing Wu, Ph.D., Karl Insogna, M.D., and Richard P. Lifton, M.D., Ph.D.High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5 N Engl J Med. 2002 May 16;346(20):1513-21.
6. Balemans W, Ebeling M, Patel N, Van Hul E, Olson P, Dioszegi M, Lacza C, Wuyts W, Van Den Ende J, Willems P, Paes-Alves AF, Hill S, Bueno M, Ramos FJ, Tacconi P, Dikkers FG, Stratakis C, Lindpaintner K, Vickery B, Foernzler D, Van Hul W.Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST) Human Molecular Genetics, 2001, Vol. 10, No. 5 537-543.
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