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Visceral Fat-Glycation Interaction Deciphers the Hidden Roots of the Refractory Type of Osteoporosis: US Patent Review

Published in Frontiers (Volume 1, Issue 4)
Received: 14 November 2021    Accepted: 3 December 2021    Published: 9 December 2021
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Abstract

Osteoporosis is a chronic disease of the bone in the elderly causing its liability to fracture on a mild trauma. The metabolic type of osteoporosis is the commonest. Its relation with hyperinsulinemia and/or diabetes Mellitus II (DM II) is poorly understood. The most hazardous effect of either hyperinsulinemia or DM II is the glycation process. The US patent (US9801905) discovered a very important link between the glycation process and the down-regulation of the insulin receptors on the osteocytes. Moreover, it was very clear that hyperinsulinemia even without diabetic manifestations sometimes has a more dangerous effect than DM II. The possible explanation is that hyperinsulinemia may raise glucose concentration inside the tissues despite its blood level might be still within its normal range. This would come at the expense of high insulin levels that maintain blood sugar within its normal ranges. On the other hand, DM II has high blood sugar but the sugar inside the tissue may be much less in most cases. Therefore, the glycation process is more likely to occur with silent hyperinsulinemia than in DM II. Furthermore, the incidence of hyperinsulinemia is much more common than DM II. Roughly, hyperinsulinemia is at least 3 times more common than DM II. Lastly, the glycation process causes down-regulation of the insulin receptors on the cell membrane of the osteocytes leading to starvation of these cells. Subsequently, the new bone formation would be greatly reduced predisposing for osteoporosis. By this paper, the very fine link between hyperinsulinemia and osteoporosis could be updated. The new lines of treatment could also be updated according to the patented data (US9801905).

Published in Frontiers (Volume 1, Issue 4)
DOI 10.11648/j.frontiers.20210104.17
Page(s) 100-111
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Osteoporosis, Piezoelectricity, Glycation, Hyper-insulinemia, NF-kB, RANK-L

References
[1] Allison P. Drain, 2020. Matrix Molecules & their ligands. The principle of tissue engineering (5th Edition). Page 119-132.
[2] MORRIS H. SHAMOS, 1963. Piezoelectric property of the bone. Nature. (197). Page. 81.
[3] Hossam Mohamed, 2017. The use of organic sulfur, antioxidants, amino acids, and exercise in the treatment of osteoporosis. https://patents.google.com/patent/US9801905B2/en
[4] Hossam Mohamed, 2020. Understanding the dynamic relationship between the sacrificial bonds and Hossam Osteonic circulation is a breakthrough for understanding osteoporosis. Researchgate. https://www.researchgate.net/publication/355916176_Understanding_the_dynamic_relationship_between_the_Hossam_osteonic_circulation_HOC_and
_the_sacrificial_bonds_is_a_breakthrough_for_the_complete_cure_of_osteoporosis_granted_US_patent_review_US9801905
[5] Jamilah M. Hashimi, 2015. Assessment of Osteoporosis Risk Factors in Low Socioeconomic Status Hemodialysis Patients in Jeddah. World Journal of Medical Sciences 12 (4): 438-443.
[6] William D. Leslie, 2015. Why Does Rate of Bone Density Loss Not Predict Fracture Risk? Journal of clinical endocrinology and metabolism. Volume 100, Issue 2, Pages 679–683.
[7] Oddom Demontiero, 2011, Aging and bone loss: new insights for the clinician. SAGE Journal. Volume: 4 issue: 2, page(s): 61-76.
[8] Jin Hee Park, 2017. Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation. Molecules and Cells. 40 (10). Page (706-713).
[9] Hossam Mohamed, 2017. Fat radiation by laser. US patent https://patents.google.com/patent/US9433798
[10] Chaoyang Li, 2006. Trends in Hyperinsulinemia Among Nondiabetic Adults in the U.S. Diabetic Care. 29 (11). Page (2396-2402).
[11] Dylan D Thomas, 2019. Hyperinsulinemia: An Early Indicator of Metabolic Dysfunction. 1; 3 (9): 1727–1747.
[12] Matthew Shoulders, 2009 Collagen Structure & stability. Annual Review. Vol. 78: page (929-958).
[13] Maciej Pawlikowski, 2017. Electric Phenomenon in Bones as a Result of Piezoelectricity of Hydroxyapatite. Archives of clinical & biomedical research. Volume 1 (3).
[14] Peng Yu, 2017. Bone-Inspired Spatially Specific Piezoelectricity Induces Bone Regeneration. Theranostics. 7 (13) page 33387-3397.
[15] Atharva A. Poundarik, 2015. A Direct Role of Collagen Glycation in Bone Fracture. Journal of the Mechanical Behavior of Biomedical Materials Volume 52. Page 120-130.
[16] KeertikFulzele, 2010. Insulin Receptor Signaling in Osteoblasts Regulates Postnatal Bone Acquisition and Body Composition. Cell. Volume 142 (2). Page (309-319).
[17] D M Thomas, 1996. Insulin receptor expression in bone. Journal of Bone & Minerals Research. Volume 11 (9). Page 1312-1320.
[18] Yue Guo, 2016, Insulin receptor substrate-1 time-dependently regulates bone formation by controlling collagen Iα2 expression via miR-342. Federation of American Societies for Experimental Biology. Volume 30 (12). Page (4214-4226).
[19] Elise F. Morgan, 2013, The Bone Organ System: Form and Function. Osteoporosis (4th Edition). Page (3-20).
[20] Luis Cardoso, 2013. A review of recent advances in the assessment of bone porosity, permeability, and interstitial fluid flow. Journal of Biomechanics. 46 (2) pages (253-265).
[21] Hossam Mohamed, 2021, Hossam Osteonic Circulation (HOC) Deciphers the Root Causes of osteoporosis & Reveals the Hidden Secrets of the Physiological Lines of Its Treatment: US Patent Review. Frontiers. Vol 1 (4). Pages (89-99).
[22] Taishin Akiyama, 2012. RANKL-RANK interaction in immune regulatory systems. World Journal of Orthopedics. Volume 3 (9): Pages (142-150).
[23] Flaminia Bardanzellu, 2019. Once we were bacteria… mitochondria to infinity and beyond. Journal of Pediatric & Neonatal Individual Medicine. Volume 8 (1) Page 80106.
[24] Li Zhang, 2019. Role of mitochondrial calcium uniporter-mediated Ca2+ and iron accumulation in traumatic brain injury. Journal of Cellular & Molecular Medicine. Volume 23 (4). Pages (2995-3009).
[25] Judith L Flanagan, 2010. The Role of Carnitine in Diseases. Nutrition & Metabolism. Volume 7 (1). Page 1.
[26] Jennie L Walgren, 2004. Effect of R(+)α-Lipoic acid on pyruvate metabolism and fatty acid oxidation in rat hepatocytes. Clinical and Experimental Metabolism. Volume 53 (2). Page 165-173.
[27] Sunil J Wimalawansa, 2008. Nitric oxide: novel therapy for osteoporosis. Expert Opinion on Pharmacotherapy. Volume 9 (17). Pages (3025-3044).
[28] Rossella Titone, 2020. Insulin receptor preserves mitochondrial function by binding VDAC1 in insulin insensitive mucosal epithelial cells. Journal of American Society for Experimental Pathology. Volume 34 (1) Pages (754-775).
[29] Dennis M. Black, 2020, Atypical Femur Fracture Risk versus Fragility Fracture Prevention with Bisphosphonates. The New England Journal of Medicine. 383: 743-753.
[30] Kurt A. Kennel, 2009, Adverse Effects of Bisphosphonates: Implications for Osteoporosis Management. Mayo Clinic Proceedings. VOLUME 84, ISSUE 7, P632-638.
Cite This Article
  • APA Style

    Hossam Mohamed, Houda Almansour, Dalal Alsaadoun, Mariam Almansour. (2021). Visceral Fat-Glycation Interaction Deciphers the Hidden Roots of the Refractory Type of Osteoporosis: US Patent Review. Frontiers, 1(4), 100-111. https://doi.org/10.11648/j.frontiers.20210104.17

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    ACS Style

    Hossam Mohamed; Houda Almansour; Dalal Alsaadoun; Mariam Almansour. Visceral Fat-Glycation Interaction Deciphers the Hidden Roots of the Refractory Type of Osteoporosis: US Patent Review. Frontiers. 2021, 1(4), 100-111. doi: 10.11648/j.frontiers.20210104.17

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    AMA Style

    Hossam Mohamed, Houda Almansour, Dalal Alsaadoun, Mariam Almansour. Visceral Fat-Glycation Interaction Deciphers the Hidden Roots of the Refractory Type of Osteoporosis: US Patent Review. Frontiers. 2021;1(4):100-111. doi: 10.11648/j.frontiers.20210104.17

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  • @article{10.11648/j.frontiers.20210104.17,
      author = {Hossam Mohamed and Houda Almansour and Dalal Alsaadoun and Mariam Almansour},
      title = {Visceral Fat-Glycation Interaction Deciphers the Hidden Roots of the Refractory Type of Osteoporosis: US Patent Review},
      journal = {Frontiers},
      volume = {1},
      number = {4},
      pages = {100-111},
      doi = {10.11648/j.frontiers.20210104.17},
      url = {https://doi.org/10.11648/j.frontiers.20210104.17},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.frontiers.20210104.17},
      abstract = {Osteoporosis is a chronic disease of the bone in the elderly causing its liability to fracture on a mild trauma. The metabolic type of osteoporosis is the commonest. Its relation with hyperinsulinemia and/or diabetes Mellitus II (DM II) is poorly understood. The most hazardous effect of either hyperinsulinemia or DM II is the glycation process. The US patent (US9801905) discovered a very important link between the glycation process and the down-regulation of the insulin receptors on the osteocytes. Moreover, it was very clear that hyperinsulinemia even without diabetic manifestations sometimes has a more dangerous effect than DM II. The possible explanation is that hyperinsulinemia may raise glucose concentration inside the tissues despite its blood level might be still within its normal range. This would come at the expense of high insulin levels that maintain blood sugar within its normal ranges. On the other hand, DM II has high blood sugar but the sugar inside the tissue may be much less in most cases. Therefore, the glycation process is more likely to occur with silent hyperinsulinemia than in DM II. Furthermore, the incidence of hyperinsulinemia is much more common than DM II. Roughly, hyperinsulinemia is at least 3 times more common than DM II. Lastly, the glycation process causes down-regulation of the insulin receptors on the cell membrane of the osteocytes leading to starvation of these cells. Subsequently, the new bone formation would be greatly reduced predisposing for osteoporosis. By this paper, the very fine link between hyperinsulinemia and osteoporosis could be updated. The new lines of treatment could also be updated according to the patented data (US9801905).},
     year = {2021}
    }
    

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Author Information
  • Medical & Research Department, Huda Health INC, Ottawa, Canada

  • Medical & Research Department, Huda Health INC, Ottawa, Canada

  • Internal Medicine Department, College of Medicine, King Faisal University, Alahsa, Saudi Arabia

  • Department of Endocrinology, AlFaisalia Hospital, Alhafouf, Saudi Arabia

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