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Journal articles on the topic 'Bone Diabetes'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Krakauer, J. C., M. J. McKenna, N. F. Buderer, D. S. Rao, F. W. Whitehouse, and A. M. Parfitt. "Bone loss and bone turnover in diabetes." Diabetes 44, no. 7 (July 1, 1995): 775–82. http://dx.doi.org/10.2337/diabetes.44.7.775.

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2

Piscitelli, Prisco, Cosimo Neglia, Antonella Vigilanza, and Annamaria Colao. "Diabetes and bone." Current Opinion in Endocrinology, Diabetes and Obesity 22, no. 6 (December 2015): 439–45. http://dx.doi.org/10.1097/med.0000000000000203.

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3

Heilmeier, Ursula, and Janina Patsch. "Diabetes and Bone." Seminars in Musculoskeletal Radiology 20, no. 03 (October 14, 2016): 300–304. http://dx.doi.org/10.1055/s-0036-1592366.

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4

Pietschmann, P., J. M. Patsch, and G. Schernthaner. "Diabetes and Bone." Hormone and Metabolic Research 42, no. 11 (August 13, 2010): 763–68. http://dx.doi.org/10.1055/s-0030-1262825.

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5

Hull, Beatrice, and Nichole R. Smith. "Diabetes and Bone." American Journal of the Medical Sciences 351, no. 4 (April 2016): 356–60. http://dx.doi.org/10.1016/j.amjms.2016.02.010.

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6

Hygum, Katrine, Jakob Starup-Linde, and Bente L. Langdahl. "Diabetes and bone." Osteoporosis and Sarcopenia 5, no. 2 (June 2019): 29–37. http://dx.doi.org/10.1016/j.afos.2019.05.001.

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7

Schwartz, A. "Diabetes and bone." Bone 44 (June 2009): S210. http://dx.doi.org/10.1016/j.bone.2009.03.038.

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8

Ferrari, Serge. "Diabetes and Bone." Calcified Tissue International 100, no. 2 (February 2017): 107–8. http://dx.doi.org/10.1007/s00223-017-0234-y.

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9

Deeba, Farah, Sidra Younis, Nida Qureshi, Tahmina Mustafa, Nadia Iqbal, and Saira Hussain. "Effect of Diabetes Mellitus and Anti-Diabetic Drugs on Bone Health-A Review." Journal of Bioresource Management 8, no. 2 (May 26, 2021): 131–48. http://dx.doi.org/10.35691/jbm.1202.0187.

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Osteoporosis and diabetes mellitus (DM) are widespread diseases and have a significant health burden. Type-1 diabetes mellitus (T1DM) and Type-2 diabetes mellitus (T2DM) are associated with an increased bone fracture. In T1DM, the increased risk of bone fracture is associated with low bone mass. In patients with T2DM, the risk of fracture of the bone is increased due to low quality of bone, despite increased bone mineral density (BMD). In type 2 diabetic patients, bone fragility depends on the quality of bone instead of a reduction in bone mass. Thiazolidinediones (TZD) cause differentiation of adipocytes and inhibit differentiation of osteoblast and bone marrow stromal stem cells (BMSC). In this review, we have described the effect of anti-diabetic drugs and diabetes mellitus on bone health and our finding shows that sulfonylureas and metformin have no negative effect on bone health and protect bones against fractures.

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10

Krakauer, J. C., M. J. Mckenna, N. Fenn Buderer, D. S. Rao, F. W. Whitehouse, and A. M. Parfitt. "Bone Loss and Bone Turnover in Diabetes." Diabetes 44, no. 7 (July 1, 1995): 775–82. http://dx.doi.org/10.2337/diab.44.7.775.

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11

Luisa Isidro, M., and Belen Ruano. "Bone Disease in Diabetes." Current Diabetes Reviews 6, no. 3 (May 1, 2010): 144–55. http://dx.doi.org/10.2174/157339910791162970.

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12

Ruzicska, Éva, and Gyula Poór. "Diabetes and bone metabolism." Orvosi Hetilap 152, no. 29 (July 2011): 1156–60. http://dx.doi.org/10.1556/oh.2011.29147.

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In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions – PPARγ agonists – are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures. Orv. Hetil., 2011, 152, 1156–1160.

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13

Antonopoulou, Marianna, Gül Bahtiyar, Mary Ann Banerji, and Alan S. Sacerdote. "Diabetes and bone health." Maturitas 76, no. 3 (November 2013): 253–59. http://dx.doi.org/10.1016/j.maturitas.2013.04.004.

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14

Gordon, D. "Diabetes and the Bone." MD Conference Express 10, no. 9 (November 1, 2010): 31–32. http://dx.doi.org/10.1177/155989771009014.

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15

Grey, Andrew. "Diabetes Medications and Bone." Current Osteoporosis Reports 13, no. 1 (November 30, 2014): 35–40. http://dx.doi.org/10.1007/s11914-014-0250-z.

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16

Schacter, G. Isanne, and William D. Leslie. "Diabetes and Bone Disease." Endocrinology and Metabolism Clinics of North America 46, no. 1 (March 2017): 63–85. http://dx.doi.org/10.1016/j.ecl.2016.09.010.

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17

Al-Hariri, Mohammed. "Sweet Bones: The Pathogenesis of Bone Alteration in Diabetes." Journal of Diabetes Research 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/6969040.

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Diabetic patients have increased fracture risk. The pathogenesis underlying the status of bone alterations in diabetes mellitus is not completely understood but is multifactorial. The major deficits appear to be related to a deficit in mineralized surface area, a decrement in the rate of mineral apposition, deceased osteoid surface, depressed osteoblast activity, and decreased numbers of osteoclasts due to abnormal insulin signaling pathway. Other prominent features of diabetes mellitus are an increased urinary excretion of calcium and magnesium, accumulation of advanced glycation end products, and oxidative stress leading to sweet bones (altered bone’s strength, metabolism, and structure). Every diabetic patient should be assessed for risk factors for fractures and osteoporosis. The pathogenesis of the bone alterations in diabetes mellitus as well as their molecular mechanisms needs further study.

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18

Hamann, Christine, Stephan Kirschner, Klaus-Peter Günther, and Lorenz C. Hofbauer. "Bone, sweet bone—osteoporotic fractures in diabetes mellitus." Nature Reviews Endocrinology 8, no. 5 (January 17, 2012): 297–305. http://dx.doi.org/10.1038/nrendo.2011.233.

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19

Rubin, Mishaela R. "Bone Cells and Bone Turnover in Diabetes Mellitus." Current Osteoporosis Reports 13, no. 3 (March 6, 2015): 186–91. http://dx.doi.org/10.1007/s11914-015-0265-0.

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20

Verhaeghe, J., E. van Herck, W. J. Visser, A. M. Suiker, M. Thomasset, T. A. Einhorn, E. Faierman, and R. Bouillon. "Bone and mineral metabolism in BB rats with long-term diabetes. Decreased bone turnover and osteoporosis." Diabetes 39, no. 4 (April 1, 1990): 477–82. http://dx.doi.org/10.2337/diabetes.39.4.477.

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21

Safarova, S. S. "Pathogenetic aspects of bone metabolism in diabetes mellitus." Clinical Medicine (Russian Journal) 96, no. 8 (December 20, 2018): 707–12. http://dx.doi.org/10.18821/0023-2149-2018-96-8-707-712.

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Metabolic disorders caused by diabetes affect bone remodeling, alter the structure and reduce the strength of bone tissue, leading to the development of diabetic osteopathy. However, between diabetes mellitus (DM) type 1 and 2 there are noticeable differences in the effect on the bone structure, which is obviously due to the different cellular and molecular mechanisms of these processes. The density of bone tissue with DM typel decreases, which leads to an increase in the risk of fractures by 7 times. With DM type 2, bone mineral density is moderately elevated, which is expected to lead to a decrease in the incidence of osteoporotic fractures, but in fact, this index is approximately doubled. Pathophysiological mechanisms underlying osteoporotic changes in diabetes mellitus are complex and included hyperglycemia, oxidative stress and accumulation of advanced glycation endproducts that alter the properties of collagen, increase fatty infiltration of the bone marrow, release inflammatory factors and adipokines from visceral adipose tissue and potentially change the function osteoblasts. Additional factors are, some antidiabetic drugs that directly affect the metabolism of bones and minerals (such as thiazolidinediones), as well as an increased tendency to fall due to micro- and macroangiopathies, all contribute to an increased risk of low-fracture fractures in patients with diabetes mellitus.

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22

Krakauer, J. C., M. J. McKenna, D. S. Rao, and F. W. Whitehouse. "Bone Mineral Density in Diabetes." Diabetes Care 20, no. 8 (August 1, 1997): 1339–40. http://dx.doi.org/10.2337/diacare.20.8.1339b.

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23

Obermayer-Pietsch, Barbara, Vito Francic, Christoph Haudum, Valentin Borzan, Natascha Schweighofer, Angelo Ascani, and Ines Foessl. "Diabetoporosity—diabetes and the bone." Journal of Laboratory and Precision Medicine 3 (December 2018): 98. http://dx.doi.org/10.21037/jlpm.2018.11.02.

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24

Kasperk, Christian, Carmen Georgescu, and Peter Nawroth. "Diabetes Mellitus and Bone Metabolism." Experimental and Clinical Endocrinology & Diabetes 125, no. 04 (January 10, 2017): 213–17. http://dx.doi.org/10.1055/s-0042-123036.

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25

Kanazawa, Ippei, and Toshitsugu Sugimoto. "Diabetes Mellitus-induced Bone Fragility." Internal Medicine 57, no. 19 (October 1, 2018): 2773–85. http://dx.doi.org/10.2169/internalmedicine.0905-18.

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26

Leslie, William D., Mishaela R. Rubin, Ann V. Schwartz, and John A. Kanis. "Type 2 diabetes and bone." Journal of Bone and Mineral Research 27, no. 11 (September 28, 2012): 2231–37. http://dx.doi.org/10.1002/jbmr.1759.

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27

Voelker, Rebecca. "Diabetes Drug Poses Bone Risks." JAMA 314, no. 15 (October 20, 2015): 1554. http://dx.doi.org/10.1001/jama.2015.13009.

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28

Greenhill, Claire. "Bone healing in diabetes mellitus." Nature Reviews Endocrinology 13, no. 3 (January 30, 2017): 128. http://dx.doi.org/10.1038/nrendo.2017.5.

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29

Hadjidakis, D., U. Lempert, H. Minne, and R. Ziegler. "Bone Loss in Experimental Diabetes." Hormone and Metabolic Research 25, no. 02 (February 1993): 77–81. http://dx.doi.org/10.1055/s-2007-1002047.

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30

Schwartz, Ann V., and Deborah E. Sellmeyer. "Diabetes, fracture, and bone fragility." Current Osteoporosis Reports 5, no. 3 (September 2007): 105–11. http://dx.doi.org/10.1007/s11914-007-0025-x.

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31

Saito, Mitsuru, Yoshikuni Kida, Soki Kato, and Keishi Marumo. "Diabetes, Collagen, and Bone Quality." Current Osteoporosis Reports 12, no. 2 (March 13, 2014): 181–88. http://dx.doi.org/10.1007/s11914-014-0202-7.

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32

Kim, Tiffany Y., and Anne L. Schafer. "Diabetes and Bone Marrow Adiposity." Current Osteoporosis Reports 14, no. 6 (October 6, 2016): 337–44. http://dx.doi.org/10.1007/s11914-016-0336-x.

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33

Moreira, C. A., and D. W. Dempster. "Bone histomorphometry in diabetes mellitus." Osteoporosis International 26, no. 11 (August 5, 2015): 2559–60. http://dx.doi.org/10.1007/s00198-015-3258-z.

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34

Lee, Eun-Jung, Woojin Na, Min-Kyung Kang, Yun-Ho Kim, Dong-Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, et al. "Hydroxycoumarin Scopoletin Inhibits Bone Loss through Enhancing Induction of Bone Turnover Markers in a Mouse Model of Type 2 Diabetes." Biomedicines 9, no. 6 (June 7, 2021): 648. http://dx.doi.org/10.3390/biomedicines9060648.

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Diabetes induces bone deterioration, which leads to increased risk of fracture, osteopenia, and osteoporosis. Thus, diabetes-associated bone fragility has been recognized as a diabetic complication. However, the pathophysiological effects of hyperglycemia on bone turnover remain unclear. Literature evidence demonstrates that anti-diabetic medications increase the risk of fractures in individuals with type 2 diabetes. Scopoletin is a naturally occurring hydroxycoumarin potentially exhibiting anti-inflammatory and antioxidant activities and ameliorating insulin resistance as an anti-diabetic agent. However, little is known regarding the effects of scopoletin on the impairment of bone remodeling that is caused by diabetes. The aim of this study was to identify that scopoletin was capable of inhibiting the impairment of bone remodeling and turnover in a mouse model of type 2 diabetes. Submicromolar scopoletin accelerated the formation TRAP-positive multinucleated osteoclasts (40.0 vs. 105.1%) and actin ring structures impaired by 33 mM glucose. Further, 1–20 μM scopoletin enhanced bone resorption and the induction of matrix-degrading enzymes in diabetic osteoclasts. The oral administration of 10 mg/kg scopoletin elevated serum RANKL/OPG ratio and osteocalcin level reduced in db/db mice along with an increase in BMD by ~6–14%; however, it was not effective in lowering blood glucose and hemoglobin glycation. In addition, the supplementation of scopoletin elevated the formation of trabecular bones and collagen fibers in femoral epiphysis and metaphysis with a thicker epiphyseal plate and cortical bones. Furthermore, 1–20 μM scopoletin enhanced ALP activity (4.39 vs. 7.02 nmol p-nitrophenyl phosphate/min/mg protein) and deposits of mineralized bone nodules in cultured osteoblasts reduced by 33 mM glucose. The treatment of diabetic osteoblasts with scopoletin stimulated the cellular induction of BMP-2 and osteopontin and Runx2 transcription. Accordingly, the administration of scopoletin protected mice from type 2 diabetes-associated bone loss through boosting bone remodeling via the robust induction of bone turnover markers of both osteoclasts and osteoblasts. These findings suggest that scopoletin could be a potential osteoprotective agent for the treatment of diabetes-associated bone loss and fractures.

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35

Gilbert, Matthew P., and Richard E. Pratley. "The Impact of Diabetes and Diabetes Medications on Bone Health." Endocrine Reviews 36, no. 2 (March 4, 2015): 194–213. http://dx.doi.org/10.1210/er.2012-1042.

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Abstract Patients with type 2 diabetes mellitus (T2DM) have an increased risk of fragility fractures despite increased body weight and normal or higher bone mineral density. The mechanisms by which T2DM increases skeletal fragility are unclear. It is likely that a combination of factors, including a greater risk of falling, regional osteopenia, and impaired bone quality, contributes to the increased fracture risk. Drugs for the treatment of T2DM may also impact on the risk for fractures. For example, thiazolidinediones accelerate bone loss and increase the risk of fractures, particularly in older women. In contrast, metformin and sulfonylureas do not appear to have a negative effect on bone health and may, in fact, protect against fragility fracture. Animal models indicate a potential role for incretin hormones in bone metabolism, but there are only limited data on the impact of dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 agonists on bone health in humans. Animal models also have demonstrated a role for amylin in bone metabolism, but clinical trials in patients with type 1 diabetes with an amylin analog (pramlintide) have not shown a significant impact on bone metabolism. The effects of insulin treatment on fracture risk are inconsistent with some studies showing an increased risk and others showing no effect. Finally, although there is limited information on the latest class of medications for the treatment of T2DM, the sodium-glucose co-transporter-2 inhibitors, these drugs do not seem to increase fracture risk. Because diabetes is an increasingly common chronic condition that can affect patients for many decades, further research into the effects of agents for the treatment of T2DM on bone metabolism is warranted. In this review, the physiological mechanisms and clinical impact of diabetes treatments on bone health and fracture risk in patients with T2DM are described.

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36

Piepkorn, B., P. Kann, T. Forst, J. Andreas, A. Pfützner, and J. Beyer. "Bone Mineral Density and Bone Metabolism in Diabetes Mellitus." Hormone and Metabolic Research 29, no. 11 (November 1997): 584–91. http://dx.doi.org/10.1055/s-2007-979106.

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37

Jackuliak, Peter, and Juraj Payer. "Osteoporosis, Fractures, and Diabetes." International Journal of Endocrinology 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/820615.

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It is well established that osteoporosis and diabetes are prevalent diseases with significant associated morbidity and mortality. Patients with diabetes mellitus have an increased risk of bone fractures. In type 1 diabetes, the risk is increased by ∼6 times and is due to low bone mass. Despite increased bone mineral density (BMD), in patients with type 2 diabetes the risk is increased (which is about twice the risk in the general population) due to the inferior quality of bone. Bone fragility in type 2 diabetes, which is not reflected by bone mineral density, depends on bone quality deterioration rather than bone mass reduction. Thus, surrogate markers and examination methods are needed to replace the insensitivity of BMD in assessing fracture risks of T2DM patients. One of these methods can be trabecular bone score. The aim of the paper is to present the present state of scientific knowledge about the osteoporosis risk in diabetic patient. The review also discusses the possibility of problematic using the study conclusions in real clinical practice.

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38

Botolin, Sergiu, and Laura R. McCabe. "Bone Loss and Increased Bone Adiposity in Spontaneous and Pharmacologically Induced Diabetic Mice." Endocrinology 148, no. 1 (January 1, 2007): 198–205. http://dx.doi.org/10.1210/en.2006-1006.

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Insulin-dependent diabetes mellitus (IDDM) is associated with increased risk of osteopenia/osteoporosis in humans. The mechanisms accounting for diabetic bone loss remain unclear. Pharmacologic inducers of IDDM, such as streptozotocin, mimic key aspects of diabetes in rodents, allow analysis at the onset of diabetes, and induce diabetes in genetically modified mice. However, side effects of streptozotocin, unrelated to diabetes, can complicate data interpretation. The nonobese diabetic (NOD) mouse model develops diabetes spontaneously without external influences, negating side effects of inducing agents. Unfortunately, in this model the onset of diabetes is unpredictable, occurs in a minority of male mice, and can only be studied in a single mouse strain. To validate the relevance of the more flexible streptozotocin-induced diabetes model for studying diabetes-associated bone loss, we compared its phenotype to the spontaneously diabetic NOD model. Both models exhibited hyperglycemia and loss of body, fat pad, and muscle weight. Furthermore, these genetically different and distinct models of diabetes induction demonstrated similar bone phenotypes marked by significant trabecular bone loss and increased bone marrow adiposity. Correspondingly, both diabetic models exhibited decreased osteocalcin mRNA and increased adipocyte fatty acid-binding protein 2 mRNA levels in isolated tibias and calvaria. Taken together, multiple streptozotocin injection-induced diabetes is a valid model for understanding the acute and chronic pathophysiologic responses to diabetes and their mechanisms in bone.

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39

Tonkikh, O. S., Yu G. Samoilova, V. D. Zavadovskaya, Ye B. Kravets, O. Yu Kilina, and L. A. Kriulko. "Diagnostic aspects of osteopenic syndrome in Type 1 pancreatic diabetes patients." Bulletin of Siberian Medicine 9, no. 5 (October 28, 2010): 165–69. http://dx.doi.org/10.20538/1682-0363-2010-5-165-169.

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The condition of a bone fabric at 102 sick diabetes mellitus type 1 (48 men and 54 women, middle age (38,2 ± 12,2) years) is studied, also are specified influence of various factors on development osteopenic syndrome. Research methods included clinical and history of development of disease, beam, biochemical, statistical methods of processing of results. As a result of research it has been revealed that indicators of bone durability at sick of a diabetes corresponded osteopenia which was accompanied by infringement micro-arhcitecture bones in the form of decrease in relative volume trabecular bones and quantities trabecula. Osteosonographie it was accompanied by changes of markers of a bone metabolism (osteocalcin and C-trailer tilopeptid) testifying to activation of processes osteolysis at sick of a diabetes.

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40

Valkusz, Zsuzsanna. "Diabetes and osteoporosis." Orvosi Hetilap 152, no. 29 (July 2011): 1161–66. http://dx.doi.org/10.1556/oh.2011.29154.

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Over the last decades a considerable amount of data has accumulated to indicate that metabolic and endocrine alterations of diabetes affect bone quantity and quality. These skeletal changes may increase the risk of bone fracture. There is strong evidence that in type 1 diabetes the decreased bone mass, lack of insulin and insulin-like growth factor-1, dysregulation of adipokines, and increased levels of proinflammatory cytokines are in the background of fragility fractures. In type 2 diabetes hyperinsulinemia, insulin resistance and increased body weight may result in an increase of bone mass; however, accumulation of advanced glycation end products within the bone collagen driven by glucotoxicity may increase the cortical porosity. There is a higher incidence of falls resulting from diabetes-related co-morbidities such as diabetic retinopathy, peripheral neuropathy, hypoglycemic episodes and sometimes from the medications. Vitamin D deficiency has special impact on glucose metabolism and the prevalence of diabetes. Vitamin D supplementation in childhood can decrease incidence of type 1 diabetes by 80%. The effect of thiazolidinediones, glucagon-like peptide-1 agonists and metformin, agents for treatment of diabetes open a new connection between bone, carbohydrate and fat metabolism. Orv. Hetil., 2011, 152, 1161–1166.

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41

Catanzaro, Orlando. "Diabetic oxidative stress and bone loss complications." Endocrinology and Disorders 5, no. 1 (March 5, 2021): 01–04. http://dx.doi.org/10.31579/2640-1045/056.

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Diabetes mellitus is a group of metabolic disorder characterize by and absolute or partial insulin deficiency. Diabetic hyperglycemia is produce by the effect of homeostasis between proteolytic enzymes, their inhibitors and the antioxidants defense that protect and repair vital tissues and molecular components. Bone consist of both component and trabecular bone tissue. Organic matrix and albumin form part of noncollagenous of bone .Initiation of mineralization and collagen fibrils form the phase of mineral matrix. Calcium flux into and out of bone depend of osteoclastic and osteoblastic activity. The remodeling is initiated by resorption and new bone formation at the resorption site. Diabetic complication is a critical factor for bone pathology and could start early inflammatory stage even before hyperglycemia. Diabetic produces bone loss from reduce osteoblast activity. Partly insulin deficiency produce defective bone remodeling indirect by oxidative stress. The current treatment for defective bone in diabetes state include biophosphonate and cinaciguat. Biphosphonate inhibit bone resorption, but may worsen bone quality. A novel type of activation of sGMP is cinaciguat an NO independent activator of oxidative GC, increase c GMP synthesis on diabetic and restore proliferation and survival of osteoblasts. Chronic hyperglycemia interferes with the oseointegration of implants in diabetics. Both diabetic and aging plays a role in abnormal differentiation of osteroblasts. In diabetic patients may improve the oral health to have a positive impact if optimal glycemic control is emphasized. However with cinaciguat present as a novel paradigm enhancing bone formation under hyperglycemia and protect bone implants.

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42

Nurullina, Guzel M., and Guzyal I. Akhmadullina. "Features of bone metabolism in diabetes mellitus." Osteoporosis and Bone Diseases 20, no. 3 (April 24, 2018): 82–89. http://dx.doi.org/10.14341/osteo2017382-89.

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Patients with diabetes mellitus (DM) have an increased risk of osteoporotic fractures, which is associated with a bone fragility. Accumulation of advanced glycation end products, hyperhomocysteinemia causes increased apoptosis of osteocytes, decreased bone formation and bone remodeling in DM. Adiponectin stimulates osteocalcin expression and osteoblast differentiation through the activation of AMPK. AMPK-activation stimulates differentiation and mineralization of osteoblasts. Hypoadiponectinemia, which is often observed in obesity and diabetes, can causes bone fragility. Diabetes mellitus is a state of low bone turnover, which is confirmed by decreased markers of bone formation (osteocalcin, P1NP), decreased markers of bone resorption (CTX, TRAP), increased regulatory markers of bone remodeling (OPG, sclerostin). Thus, the study of the pathophysiology of bone metabolism, the level of bone metabolism markers in patients with diabetes mellitus gives broad prospects in understanding the mechanisms of osteoporosis as complication of diabetes mellitus, the selection of targeted therapy and the improvement of early diagnosis of the disease.

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43

Elamir, Yasmine, Arianna L. Gianakos, Joseph M. Lane, Anupa Sharma, William P. Grist, Frank A. Liporace, and Richard S. Yoon. "The Effects of Diabetes and Diabetic Medications on Bone Health." Journal of Orthopaedic Trauma 34, no. 3 (March 2020): e102-e108. http://dx.doi.org/10.1097/bot.0000000000001635.

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44

Epstein, S., G. Defeudis, S. Manfrini, N. Napoli, and P. Pozzilli. "Diabetes and disordered bone metabolism (diabetic osteodystrophy): time for recognition." Osteoporosis International 27, no. 6 (March 15, 2016): 1931–51. http://dx.doi.org/10.1007/s00198-015-3454-x.

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45

Ponyrko, A. O. "THE EFFECT OF CHRONIC HYPERGLYCEMIA ON THE STATE OF MUSCULOSKELETAL SYSTEM (LITERATURE REVIEW)." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 21, no. 1 (March 21, 2021): 184–87. http://dx.doi.org/10.31718/2077-1096.21.1.184.

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Diabetes mellitus is a metabolic disorder that today has become a threatening problem for human health. Its prevalence has been constantly increasing throughout the world over the past decades. Diabetes mellitus is regarded as an incurable metabolic disorder characterized by hyperglycemia, which is caused by defects in insulin secretion. This disease annually affects almost 3% of the total population of the planet. Chronic hyperglycemia causes dysfunction of various organs of the body, such as the eyes, kidneys, heart, blood vessels, and nerves. The most common complications of diabetes include lesions of the vessels of the eye, kidneys, lower limbs and nervous system. A high level of glucose in the blood causes the development of a wide range of pathological disorders, which affect bones as well. Recent studies have shown that diseases of the skeletal system are often observed in diabetes mellitus. Speaking about the effect of hyperglycemia on bones, the development of osteopenia and osteoporosis should be noted. In this regard, an important area of research is to study changes in the bone tissue in patients with type 1 diabetes mellitus and the mechanisms that lead to disruption of bone structure and metabolism. The article highlights the pathophysiological mechanisms of hyperglycemia action in type 1 diabetes that explains complex disorders of the organs of the musculoskeletal system. The detrimental effect of hyperglycemia results in marked degenerative changes in bone cells. The pathogenic effect of hyperglycemia on bone tissue is manifested in a decrease in bone mineral density that is due to the lack of insulin and, as a consequence, significant metabolic disorders, a decrease in bone mass, inhibition of bone tissue formation, a significant decrease in the trace element composition of bone. The combination of these factors creates the appropriate pathomorphological basis for the development of diabetic osteopathy. The article highlights the mechanism of action of hyperglycemia on skeletal system in order to stimulate to a more detailed investigation of diabetes mellitus in experimental animals.

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Costantini, Silvia, and Caterina Conte. "Bone health in diabetes and prediabetes." World Journal of Diabetes 10, no. 8 (August 15, 2019): 421–45. http://dx.doi.org/10.4239/wjd.v10.i8.421.

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Mascarenhas, Mário Rui, Ana Paula Barbosa, Nuno Duarte, Ana Wessling, José Poupino, Raquel Paixão, David Barbosa, et al. "PP05. Diabetes mellitus and bone mass." Revista Portuguesa de Endocrinologia, Diabetes e Metabolismo 11 (June 2016): 2–3. http://dx.doi.org/10.1016/s1646-3439(16)30029-3.

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Shah, Viral N., R. Dana Carpenter, Virginia L. Ferguson, and Ann V. Schwartz. "Bone health in type 1 diabetes." Current Opinion in Endocrinology & Diabetes and Obesity 25, no. 4 (August 2018): 231–36. http://dx.doi.org/10.1097/med.0000000000000421.

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Moseley, Kendall F. "Type 2 diabetes and bone fractures." Current Opinion in Endocrinology & Diabetes and Obesity 19, no. 2 (April 2012): 128–35. http://dx.doi.org/10.1097/med.0b013e328350a6e1.

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Suzuki, Kiyoshi, Makoto Takizawa, Eiji Itagaki, and Hitoshi Ishida. "Diabetes Mellitus and Metabolic Bone Disorder." Japanese Journal of Nutrition and Dietetics 57, no. 3 (1999): 125–34. http://dx.doi.org/10.5264/eiyogakuzashi.57.125.

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