糖尿病与骨质疏松相关性研究进展
Research Progress on Correlation between Diabetes Mellitus and Osteoporosis
DOI: 10.12677/ACM.2022.125704, PDF,  被引量   
作者: 赵 鹏:内蒙古民族大学,内蒙古 通辽;张春香:内蒙古林业总医院,内蒙古 牙克石
关键词: 糖尿病相关性骨质疏松机制药物Diabetes Mellitus Correlation Osteoporosis Mechanism Drug
摘要: 糖尿病(DM, diabetes mellitus)和骨质疏松症(OP, osteoporosis)是两种有差异的疾病,有不同的并发症。长期慢性高血糖的刺激引起、脂质沉积、血供差、葡萄糖毒性以及氧化应激的联合作用可导致骨质疏松的发生;除了糖尿病患者可以发生骨质疏松,其他导致或缓解糖尿病的药物也可以引起骨质疏松;例如:皮质醇激素,免疫抑制剂,利尿剂,降钙素等药物有着相似的致病途径。目的:从发病机制和药物相互作用研究糖尿病与骨质疏松相关性。
Abstract: Diabetes mellitus (DM) and osteoporosis (OP) are two different diseases with different complica-tions. The combined effects of chronic hyperglycemia, lipid deposition, poor blood supply, glucose toxicity and oxidative stress can lead to osteoporosis. In addition to diabetes patients, other drugs that cause or relieve diabetes can also cause osteoporosis; Drugs such as cortisol, immunosuppres-sants, diuretics, and calcitonin have similar pathways. Objective: To study the relationship between diabetes mellitus and osteoporosis from the perspective of pathogenesis and drug interaction.
文章引用:赵鹏, 张春香. 糖尿病与骨质疏松相关性研究进展[J]. 临床医学进展, 2022, 12(5): 4858-4863. https://doi.org/10.12677/ACM.2022.125704

参考文献

[1] Liu, C., Lyu, H., Niu, P., Tan, J. and Ma, Y. (2020) Association between Diabetic Neuropathy and Osteoporosis in Pa-tients: A Systematic Review and Meta-Analysis. Archives of Osteoporosis, 15, Article No. 125. [Google Scholar] [CrossRef] [PubMed]
[2] Lotfy, M., Adeghate, J., Kalasz, H., Singh, J. and Adeghate, E. (2017) Chronic Complications of Diabetes Mellitus: A Mini Review. Current Diabetes Reviews, 13, 3-10. [Google Scholar] [CrossRef] [PubMed]
[3] Kolluru, G.K., Bir, S.C. and Kevil, C.G. (2012) En-dothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing. International Journal of Vascular Medicine, 2012, Article ID: 918267. [Google Scholar] [CrossRef] [PubMed]
[4] Hayyan, M., Hashim, M.A. and Al Nashef, I.M. (2016) Superoxide Ion: Generation and Chemical Implications. Chemical Reviews, 116, 3029-3085. [Google Scholar] [CrossRef] [PubMed]
[5] Saito, M., Fujii, K., Soshi, S., et al. (2006) Reductions in Degree of Mineralization and Enzymatic Collagen Cross- Links and Increases in Glycation-Induced Pentosidine in the Femoral Neck Cortex in Cases of Femoral Neck Fracture. Osteoporosis International, 17, 986-995. [Google Scholar] [CrossRef] [PubMed]
[6] Li, G., Xu, J. and Li, Z. (2012) Receptor for Advanced Glycation End Products Inhibits Proliferation in Osteoblast through Suppression of Wnt, PI3K and ERK Signaling. Biochemical and Biophysical Research Communications, 423, 684-689. [Google Scholar] [CrossRef] [PubMed]
[7] Ding, K.H., Wang, Z.Z., Hamrick, M.W., et al. (2006) Disordered Osteoclast Formation in RAGE Deficient Mouse Establishes an Essential Role for RAGE in Diabetes Related Bone Loss. Biochemical and Biophysical Research Communications, 340, 1091-1097. [Google Scholar] [CrossRef] [PubMed]
[8] Hein, G.E. (2006) Glycation Endproducts in Osteoporosis—Is There a Pathophysiologic Importance? Clinica Chimica Acta, 371, 32-36. [Google Scholar] [CrossRef] [PubMed]
[9] Patel, R., Shervington, A., Pariente, J.A., et al. (2006) Mechanism of Exocrine Pancreatic Insufficiency in Streptozotocin-Induced Yype 1 Diabetes Mellitus. Annals of the New York Academy of Sciences, 1084, 71-88. [Google Scholar] [CrossRef] [PubMed]
[10] Chen, H. and Li, J. (2018) Wang Q Associations between Bone-Alkaline Phosphatase and Bone Mineral Density in Adults with and without Diabetes. Medicine, 97, Article ID: e0432. [Google Scholar] [CrossRef
[11] Ala, M., Jafari, R.M. and Dehpour, A.R. (2020) Di-abetes Mellitus and Osteoporosis Correlation: Challenges and Hopes. Current Diabetes Reviews, 16, 984-1001. [Google Scholar] [CrossRef] [PubMed]
[12] Adler, R. A., et al. (2013) Glucocorticoid-Induced Osteoporosis. In: Marcus, R. et al., Eds., Osteoporosis, Academic Press, Cambridge, MA, 1191-1223. [Google Scholar] [CrossRef
[13] Darjani, A., Nickhah, N., Hedayati Emami, M.H., et al. (2017) Assessment of the Prevalence and Risk Factors Associated with GlucocorticoidInduced Diabetes Mellitus in Pemphigus Vulgaris Patients. Acta Medica Iranica, 55, 375-380.
[14] Weinstein, R.S., Jilka, R.L., Parfitt, A.M. and Manolagas, S.C. (1998) Inhibition of Osteoblastogenesis and Promotion of Apoptosis of Osteoblasts and Osteocytes Byglucocorticoids. Potential Mechanisms of Their Deleterious Effects on Bone. Journal of Clinical Investigation, 102, 274-282. [Google Scholar] [CrossRef
[15] Almeida, M., Han, L., Ambrogini, E., Weinstein, R.S. and Mano-lagas, S.C. (2011) Glucocorticoids and Tumor Necrosis Factor α Increase Oxidative Stress and Suppress Wnt Protein Signaling in Osteoblasts. Journal of Biological Chemistry, 286, 44326-44335. [Google Scholar] [CrossRef
[16] Jagpal, A., De, S.D., Singh, S.A. and Kirk, A. (2018) Is Tacrolimus More Likely to Induce Diabetes Mellitus Than Ciclosporin in Heart Transplant Patients? Vessel Plus, 2, Article No. 24. [Google Scholar] [CrossRef
[17] Velleca, A., Kittleson, M., Patel, J., Rafiei, M., Osborne, A., Ngan, A., et al. (2013) Tacrolimus-Versus Cyclosporine- Induced Diabetes Leads to More Diabetic Complications after Heart Transplantation. The Journal of Heart and Lung Transplantation, 32, S202. [Google Scholar] [CrossRef
[18] Baran, D., Ashkar, J., Galin, I., Sandler, D., Segura, L., Court-ney, M., et al. (2002) Tacrolimus and New Onset Diabetes Mellitus: The Effect of Steroid Weaning. Transplantation Proceedings, 34, 1711-1712. [Google Scholar] [CrossRef
[19] Li, Z., Sun, F., Zhang, Y., et al. (2015) Tacrolimus Induces Insulin Resistance and Increases the Glucose Absorption in the Jejunum: A Potential Mechanism of the Diabetogenic Ef-fects. PLoS ONE, 10, Article ID: e0143405. [Google Scholar] [CrossRef] [PubMed]
[20] Rodríguez-Rodríguez, A.E., Triñanes, J., Porrini, E., et al. (2015) Glucose Homeostasis Changes and Pancreatic β-Cell Proliferation after Switching to Cyclosporin in Tacroli-mus-Induced Diabetes Mellitus. Nefrologia, 35, 264-272. [English Edition]. [Google Scholar] [CrossRef
[21] Triñanes, J., Rodriguez-Rodriguez, A.E., Brito-Casillas, Y., et al. (2017) Deciphering Tacrolimus-Induced Toxicity in Pancreatic β Cells. American Journal of Transplantation, 17, 2829-2840. [Google Scholar] [CrossRef] [PubMed]
[22] Sheu, A. and Diamond, T. (2016) Secondary Osteoporosis. Australian Prescriber, 39, 85-87. [Google Scholar] [CrossRef] [PubMed]
[23] Spolidorio, L.C., Nassar, P.O., Nassar, C.A., Spolidorio, D.M. and Muscará, M.N. (2007) Conversion of Immunosuppressive Monotherapy from Cyclosporin A to Tacrolimus Re-verses Bone Loss in Rats. Calcified Tissue International, 81, 114-123. [Google Scholar] [CrossRef] [PubMed]
[24] Ponticelli, C., Aroldi, A., Goffin, E., Devendra, D. and Wilkin, T. (2001) Osteoporosis after Organ Transplantation. Lancet, 357, 1623. [Google Scholar] [CrossRef
[25] Martin-Fernandez, M., Rubert, M., Montero, M. and De La Piedra, C. (2017) Effects of Cyclosporine, Tacrolimus, and Rapamycin on Osteoblasts Transplantation Proceedings, 49, 2219-2224. [Google Scholar] [CrossRef] [PubMed]
[26] Smallwood, G., Burns, D., Fasola, C., Steiber, A. and Heffron, T. (2005) Relationship between Immunosuppression and Osteoporosis in an Outpatient Liver Transplant Clinic. Transplantation Proceedings, 37, 1910-1911. [Google Scholar] [CrossRef] [PubMed]
[27] Goldner, M.G., Zarowitz, H. and Akgun, S. (1960) Hy-perglycemia and Glycosuria Due to Thiazide Derivatives Administered in Diabetes Mellitus. New England Journal of Medicine, 262, 403-405. [Google Scholar] [CrossRef
[28] Scheen, A.J. (2018) Type 2 Diabetes and Thiazide Diuretics. Current Diabetes Reports, 18, Article No. 6. [Google Scholar] [CrossRef] [PubMed]
[29] Zillich, A.J., Garg, J., Basu, S., Bakris, G.L. and Carter, B.L. (2006) Thiazide Diuretics, Potassium, and the Development of Diabetes: A Quantitative Review. Hypertension, 48, 219-224. [Google Scholar] [CrossRef
[30] Shafi, T., Appel, L.J., Miller III, E.R., Klag, M.J. and Parekh, R.S. (2008) Changes in Serum Potassium Mediate Thiazide-Induced Diabetes. Hypertension, 52, 1022-1029. [Google Scholar] [CrossRef
[31] Rapoport, M.I. and Hurd, H.F. (1964) Thia-zide-Induced Glucose Intolerance Treated with Potassium. Archives of Internal Medicine, 113, 405-408. [Google Scholar] [CrossRef] [PubMed]
[32] Helderman, J.H., Elahi, D., Andersen, D.K., Raizes, G.S., Tobin, J.D., Shocken, D., et al. (1986) Prevention of the Glucose Intolerance of Thiazide Diuretics by Maintenance of Body-Potassium. In: Krück, F. and Schrey, A., Eds., Diuretika III, Springer, Berlin, Heidelberg, 98-109. [Google Scholar] [CrossRef
[33] Brown, M.J., Williams, B., Morant, S.V., et al. (2016) Effect of Amiloride, or Amiloride plus Hydrochlorothiazide, Versus Hydrochlorothiazide on Glucose Tolerance and Blood Pressure (PATHWAY-3): A Parallelgroup, Double-Blind Randomised Phase 4 Trial. The Lancet Diabetes & Endocri-nology, 4, 136-147. [Google Scholar] [CrossRef
[34] Transbøl, I., Christensen, M.S., Jensen, G.F., Christiansen, C. and McNair, P. (1982) Thiazide for the Postponement of Postmenopausal Bone Loss. Metabolism, 31, 383-386. [Google Scholar] [CrossRef] [PubMed]
[35] Cauley, J.A., Cummings, S.R., Seeley, D.G., et al. (1993) Ef-fects of Thiazide Diuretic Therapy on Bone Mass, Fractures, and Falls. Annals of Internal Medicine, 118, 666-673. [Google Scholar] [CrossRef] [PubMed]
[36] Xiao, X., Xu, Y. and Wu, Q. (2018) Thiazide Diuretic Usage and Risk of Fracture: A Meta-Analysis of Cohort Studies. Osteoporosis International, 29, 1515-1524. [Google Scholar] [CrossRef] [PubMed]
[37] Legroux-Gerot, I., Catanzariti, L., Marchandise, X., Duquesnoy, B. and Cortet, B. (2004) Bone Mineral Density Changes in Hypercalciuretic Osteo Porotic Men Treated with Thiazide Diuretics. Joint Bone Spine, 71, 51-55. [Google Scholar] [CrossRef] [PubMed]
[38] Kruse, C., Eiken, P. and Vestergaard, P. (2016) Continuous and Long-Term Treatment Is More Important Than Dosage for the Protective Effect of Thiazide Use on Bone Metabolism and Fracture Risk. Journal of Internal Medicine, 279, 110-122. [Google Scholar] [CrossRef] [PubMed]
[39] Cheng, L., Zhang, K. and Zhang, Z. (2018) Effectiveness of Thiazides on Serum and Urinary Calcium Levels and Bone Mineral Density in Patients with Osteoporosis: A Systematic Review and Meta-Analysis. Drug Design, Development and Ther-apy, 12, 3929-3235. [Google Scholar] [CrossRef
[40] Mefford, I.N. and Wade, E.U. (2009) Proton Pump Inhibitors as a Treatment Method for Type II Diabetes. Medical Hypotheses, 73, 29-32. [Google Scholar] [CrossRef] [PubMed]
[41] Suarez-Pinzon, W.L., Cembrowski, G.S. and Rabinovitch, A. (2009) Combination Therapy with A Dipeptidyl Peptidase-4 Inhibitor and A Proton Pump Inhibitor Restores Normogly-caemia in Non-Obese Diabetic Mice. Diabetologia, 52, 1680-1682. [Google Scholar] [CrossRef] [PubMed]
[42] Crouch, M.A., Mefford, I.N. and Wade, E.U. (2012) Proton Pump Inhibitor Therapy Associated with Lower Glycosylated Hemoglobin Levels in Type 2 Diabetes. Journal of the American Board of Family Medicine, 25, 50-54. [Google Scholar] [CrossRef] [PubMed]
[43] Inci, F., Atmaca, M., Ozturk, M., et al. (2014) Pantoprazole May Improve Beta Cell Function and Diabetes Mellitus. Journal of Endocrinological Investigation, 37, 449-454. [Google Scholar] [CrossRef] [PubMed]
[44] Singh, P.K., Hota, D., Dutta, P., et al. (2012) Pantoprazole Im-proves Glycemic Control in Type 2 Diabetes: A Randomized, Double-Blind, Placebocontrolled Trial. Journal of Clinical Endocrinology & Metabolism, 97, E2105-E2108. [Google Scholar] [CrossRef] [PubMed]
[45] Lin, H.-C., Hsiao, Y.-T., Lin, H.-L., et al. (2016) The Use of Proton Pump Inhibitors Decreases the Risk of Diabetes Mellitus in Patients with Upper Gastrointestinal Disease: A Popula-tion-Based Retrospective Cohort Study. Medicine, 95, E4195. [Google Scholar] [CrossRef
[46] Suarez-Pinzon, W.L., Lakey, J.R. and Rabinovitch, A. (2008) Combination Therapy with Glucagon-Like Peptide-1 and Gastrin Induces β-Cell Neogenesis from Pancreatic Duct Cells in Human Islets Transplanted in Immunodeficient Diabetic Mice. Cell Transplant, 17, 631-640. [Google Scholar] [CrossRef] [PubMed]
[47] Suarez-Pinzon, W.L. and Rabinovitch, A. (2011) Combination Therapy with A Dipeptidyl Peptidase-4 Inhibitor and A Proton Pump Inhibitor Induces β-Cell Neogenesis from Adult Human Pancreatic Duct Cells Implanted in Immunodeficient Mice. Cell Transplant, 20, 1343-1349. [Google Scholar] [CrossRef
[48] Abbasi, A., Corpeleijn, E., Postmus, D., et al. (2010) Plasma Procalcitonin Is Associated with Obesity, Insulin Resistance, and the Metabolic Syndrome. Journal of Clinical Endocri-nology & Metabolism, 95, E26-E31. [Google Scholar] [CrossRef] [PubMed]
[49] Hjuler, S.T., Gydesen, S., Andreassen, K.V., Karsdal, M.A. and Hen-riksen, K. (2017) The Dual Amylin- and Calcitonin-Receptor Agonist KBP-042 Works as Adjunct to Metformin on Fasting Hyperglycemia and HbA1c in a Rat Model of Type 2 Diabetes. Journal of Pharmacology and Experimental Therapeutics, 362, 24-30. [Google Scholar] [CrossRef] [PubMed]
[50] Andreassen, K.V., Michael Feigh, M., Hjuler, S.T., Gydesen, S., Henriksen, J.E., Beck-Nielsen, H., et al. (2014) A Novel Oral Dual Amylin and Calcitonin Receptor Agonist (KBP-042) Exerts Anti-Obesity and Antidiabetic Effects in Rats. American Journal of Physiology - Endocrinology and Metabolism, 307, E24-E33. [Google Scholar] [CrossRef] [PubMed]
[51] Binkley, N., Bolognese, M., Sidorowicz-Bialynicka, A., et al. (2012) A Phase 3 Trial of the Efficacy and Safety of Oral Recombinant Calcitonin: The Oral Calcitonin in Postmenopau-sal Osteoporosis (ORACAL) Trial. Journal of Bone and Mineral Research, 27, 1821-1829. [Google Scholar] [CrossRef] [PubMed]
[52] Zhou, H. and Seibel, M.J. (2017) Bone: Osteoblasts and Global Energy Metabolism—Beyond Osteocalcin. Nature Reviews Rheumatology, 13, 261-262. [Google Scholar] [CrossRef] [PubMed]