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Journal articles on the topic 'Bone Diseases, Metabolic – physiopathology'

Author: Grafiati

Published: 29 July 2024

Last updated: 31 July 2024

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1

Izzo, Marcello, Albino Carrizzo, Carmine Izzo, Enrico Cappello, Domenico Cecere, Michele Ciccarelli, Patrizia Iannece, Antonio Damato, Carmine Vecchione, and Francesco Pompeo. "Vitamin D: Not Just Bone Metabolism but a Key Player in Cardiovascular Diseases." Life 11, no. 5 (May 18, 2021): 452. http://dx.doi.org/10.3390/life11050452.

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Vitamin D is the first item of drug expenditure for the treatment of osteoporosis. Its deficiency is a condition that affects not only older individuals but also young people. Recently, the scientific community has focused its attention on the possible role of vitamin D in the development of several chronic diseases such as cardiovascular and metabolic diseases. This review aims to highlight the possible role of vitamin D in cardiovascular and metabolic diseases. In particular, here we examine (1) the role of vitamin D in diabetes mellitus, metabolic syndrome, and obesity, and its influence on insulin secretion; (2) its role in atherosclerosis, in which chronic vitamin D deficiency, lower than 20 ng/mL (50 nmol/liter), has emerged among the new risk factors; (3) the role of vitamin D in essential hypertension, in which low plasma levels of vitamin D have been associated with both an increase in the prevalence of hypertension and diastolic hypertension; (4) the role of vitamin D in peripheral arteriopathies and aneurysmal pathology, reporting that patients with peripheral artery diseases had lower vitamin D values than non-suffering PAD controls; (5) the genetic and epigenetic role of vitamin D, highlighting its transcriptional regulation capacity; and (6) the role of vitamin D in cardiac remodeling and disease. Despite the many observational studies and meta-analyses supporting the critical role of vitamin D in cardiovascular physiopathology, clinical trials designed to evaluate the specific role of vitamin D in cardiovascular disease are scarce. The characterization of the importance of vitamin D as a marker of pathology should represent a future research challenge.

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2

Biver, Emmanuel, Pierre Hardouin, and Joseph Caverzasio. "The “bone morphogenic proteins” pathways in bone and joint diseases: Translational perspectives from physiopathology to therapeutic targets." Cytokine & Growth Factor Reviews 24, no. 1 (February 2013): 69–81. http://dx.doi.org/10.1016/j.cytogfr.2012.06.003.

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3

Grill, Vivian, and T. John Martin. "Metabolic bone diseases." Medical Journal of Australia 163, no. 1 (July 1995): 38–41. http://dx.doi.org/10.5694/j.1326-5377.1995.tb126087.x.

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4

SEINO, YOSHIKI. "Metabolic bone diseases." Pediatrics International 39, no. 4 (August 1997): 478. http://dx.doi.org/10.1111/j.1442-200x.1997.tb03623.x.

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5

Horvai, Andrew E., and Brendan F. Boyce. "Metabolic bone diseases." Seminars in Diagnostic Pathology 28, no. 1 (February 2011): 13–25. http://dx.doi.org/10.1053/j.semdp.2011.02.004.

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6

Dubois-Deruy, Emilie, Yara El Masri, Annie Turkieh, Philippe Amouyel, Florence Pinet, and Jean-Sébastien Annicotte. "Cardiac Acetylation in Metabolic Diseases." Biomedicines 10, no. 8 (July 29, 2022): 1834. http://dx.doi.org/10.3390/biomedicines10081834.

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Lysine acetylation is a highly conserved mechanism that affects several biological processes such as cell growth, metabolism, enzymatic activity, subcellular localization of proteins, gene transcription or chromatin structure. This post-translational modification, mainly regulated by lysine acetyltransferase (KAT) and lysine deacetylase (KDAC) enzymes, can occur on histone or non-histone proteins. Several studies have demonstrated that dysregulated acetylation is involved in cardiac dysfunction, associated with metabolic disorder or heart failure. Since the prevalence of obesity, type 2 diabetes or heart failure rises and represents a major cause of cardiovascular morbidity and mortality worldwide, cardiac acetylation may constitute a crucial pathway that could contribute to disease development. In this review, we summarize the mechanisms involved in the regulation of cardiac acetylation and its roles in physiological conditions. In addition, we highlight the effects of cardiac acetylation in physiopathology, with a focus on obesity, type 2 diabetes and heart failure. This review sheds light on the major role of acetylation in cardiovascular diseases and emphasizes KATs and KDACs as potential therapeutic targets for heart failure.

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7

Dumond Bourie, Aurore, Jean-Baptiste Potier, Michel Pinget, and Karim Bouzakri. "Myokines: Crosstalk and Consequences on Liver Physiopathology." Nutrients 15, no. 7 (March 31, 2023): 1729. http://dx.doi.org/10.3390/nu15071729.

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Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease mainly characterized by the hepatic accumulation of lipid inducing a deregulation of β-oxidation. Its advanced form is non-alcoholic steatohepatitis (NASH), which, in addition to lipid accumulation, induces hepatocellular damage, oxidative stress and fibrosis that can progress to cirrhosis and to its final stage: hepatocellular carcinoma (HCC). To date, no specific therapeutic treatment exists. The implications of organ crosstalk have been highlighted in many metabolic disorders, such as diabetes, metabolic-associated liver diseases and obesity. Skeletal muscle, in addition to its role as a reservoir and consumer of energy and carbohydrate metabolism, is involved in this inter-organs’ communication through different secreted products: myokines, exosomes and enzymes, for example. Interestingly, resistance exercise has been shown to have a beneficial impact on different metabolic pathways, such as lipid oxidation in different organs through their secreted products. In this review, we will mainly focus on myokines and their effects on non-alcoholic fatty liver disease, and their complication: non-alcoholic steatohepatitis and HCC.

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8

Sánchez-Oliver, Antonio Jesús. "Obesity Phisiopathology: Current Perspectives." Journal of Nutritional Biology 4, no. 1 (December 20, 2017): 21. http://dx.doi.org/10.18314/jnb.v4i1.160.

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Obesity is a global health problem, being considered one of the most serious and prevalent non-communicable diseases of the 21st century. It is currently understood as a multifactorial chronic condition associated with potentially serious complications whose treatment requires a multidisciplinary approach, given its huge clinical impact and associated health-carecost. Besides, properly tackling obesity requires a founded knowledge of its specific physiopathology is required. Together withthe rise in adiposity, a series of cellular processes happen, which cause several metabolic changes that drive to a vicious circle ofvisceral fat increase. This process in enhanced by genetic and environmental factors associated to multiple diseases (metabolic,cardiovascular, osteoarticular, etc.) that increase morbidity and mortality. The aim of this review is to introduce the currentperspectives on obesity physiopathology in a simple and didactic manner, in order to contribute to a better approach by thedifferent professionals that work with obesity in their everyday practice.

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9

Rossi, Francesca, Chiara Tortora, Marco Paoletta, Maria Maddalena Marrapodi, Maura Argenziano, Alessandra Di Paola, Elvira Pota, Daniela Di Pinto, Martina Di Martino, and Giovanni Iolascon. "Osteoporosis in Childhood Cancer Survivors: Physiopathology, Prevention, Therapy and Future Perspectives." Cancers 14, no. 18 (September 6, 2022): 4349. http://dx.doi.org/10.3390/cancers14184349.

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The improvement of chemotherapy, radiotherapy, and surgical interventions, together with hematopoietic stem cell transplantation, increased childhood cancer survival rate in the last decades, reaching 80% in Europe. Nevertheless, anti-cancer treatments are mainly responsible for the onset of long-term side effects in childhood cancer survivors (CCS), including alterations of the endocrine system function and activity. In particular, the most frequent dysfunction in CCS is a metabolic bone disorder characterized by low bone mineral density (BMD) with increased skeletal fragility. BMD loss is also a consequence of a sedentary lifestyle, malnutrition, and cancer itself could affect BMD, thus inducing osteopenia and osteoporosis. In this paper, we provide an overview of possible causes of bone impairment in CCS in order to propose management strategies for early identification and treatment of skeletal fragility in this population.

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10

Sinigaglia, L. "Metabolic bone diseases: an overview." Reumatismo 66, no. 2 (July 28, 2014): 109. http://dx.doi.org/10.4081/reumatismo.2014.783.

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11

Guglielmi, Giuseppe, Silvana Muscarella, Antonio Leone, and Wilfred C. G. Peh. "Imaging of Metabolic Bone Diseases." Radiologic Clinics of North America 46, no. 4 (July 2008): 735–54. http://dx.doi.org/10.1016/j.rcl.2008.04.010.

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12

Polyzos, Stergios A., and Christos S. Mantzoros. "Outliers of bone metabolic diseases." Metabolism 80 (March 2018): 1–4. http://dx.doi.org/10.1016/j.metabol.2017.09.009.

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13

Haugeberg, Glenn. "Imaging of metabolic bone diseases." Best Practice & Research Clinical Rheumatology 22, no. 6 (December 2008): 1127–39. http://dx.doi.org/10.1016/j.berh.2008.09.016.

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14

Canalis, Ernesto. "Growth Factors, Bone Metabolism, and Metabolic Bone Diseases." Endocrinologist 6, no. 2 (March 1996): 89–94. http://dx.doi.org/10.1097/00019616-199603000-00005.

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15

Parkman, Robertson, and Crooks. "BONE MARROW TRANSPLANTATION FOR METABOLIC DISEASES." Radiologic Clinics of North America 16, no. 2 (May 1996): 429–38. http://dx.doi.org/10.1016/s0033-8389(22)00219-6.

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16

Sobh, Mahmoud M., Mohamed Abdalbary, Sherouk Elnagar, Eman Nagy, Nehal Elshabrawy, Mostafa Abdelsalam, Kamyar Asadipooya, and Amr El-Husseini. "Secondary Osteoporosis and Metabolic Bone Diseases." Journal of Clinical Medicine 11, no. 9 (April 24, 2022): 2382. http://dx.doi.org/10.3390/jcm11092382.

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Fragility fracture is a worldwide problem and a main cause of disability and impaired quality of life. It is primarily caused by osteoporosis, characterized by impaired bone quantity and or quality. Proper diagnosis of osteoporosis is essential for prevention of fragility fractures. Osteoporosis can be primary in postmenopausal women because of estrogen deficiency. Secondary forms of osteoporosis are not uncommon in both men and women. Most systemic illnesses and organ dysfunction can lead to osteoporosis. The kidney plays a crucial role in maintaining physiological bone homeostasis by controlling minerals, electrolytes, acid-base, vitamin D and parathyroid function. Chronic kidney disease with its uremic milieu disturbs this balance, leading to renal osteodystrophy. Diabetes mellitus represents the most common secondary cause of osteoporosis. Thyroid and parathyroid disorders can dysregulate the osteoblast/osteoclast functions. Gastrointestinal disorders, malnutrition and malabsorption can result in mineral and vitamin D deficiencies and bone loss. Patients with chronic liver disease have a higher risk of fracture due to hepatic osteodystrophy. Proinflammatory cytokines in infectious, autoimmune, and hematological disorders can stimulate osteoclastogenesis, leading to osteoporosis. Moreover, drug-induced osteoporosis is not uncommon. In this review, we focus on causes, pathogenesis, and management of secondary osteoporosis.

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17

Sobh, Mahmoud M., Mohamed Abdalbary, Sherouk Elnagar, Eman Nagy, Nehal Elshabrawy, Mostafa Abdelsalam, Kamyar Asadipooya, and Amr El-Husseini. "Secondary Osteoporosis and Metabolic Bone Diseases." Journal of Clinical Medicine 11, no. 9 (April 24, 2022): 2382. http://dx.doi.org/10.3390/jcm11092382.

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Fragility fracture is a worldwide problem and a main cause of disability and impaired quality of life. It is primarily caused by osteoporosis, characterized by impaired bone quantity and or quality. Proper diagnosis of osteoporosis is essential for prevention of fragility fractures. Osteoporosis can be primary in postmenopausal women because of estrogen deficiency. Secondary forms of osteoporosis are not uncommon in both men and women. Most systemic illnesses and organ dysfunction can lead to osteoporosis. The kidney plays a crucial role in maintaining physiological bone homeostasis by controlling minerals, electrolytes, acid-base, vitamin D and parathyroid function. Chronic kidney disease with its uremic milieu disturbs this balance, leading to renal osteodystrophy. Diabetes mellitus represents the most common secondary cause of osteoporosis. Thyroid and parathyroid disorders can dysregulate the osteoblast/osteoclast functions. Gastrointestinal disorders, malnutrition and malabsorption can result in mineral and vitamin D deficiencies and bone loss. Patients with chronic liver disease have a higher risk of fracture due to hepatic osteodystrophy. Proinflammatory cytokines in infectious, autoimmune, and hematological disorders can stimulate osteoclastogenesis, leading to osteoporosis. Moreover, drug-induced osteoporosis is not uncommon. In this review, we focus on causes, pathogenesis, and management of secondary osteoporosis.

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18

Kara Gedik, Gonca. "Radionuclide Imaging in Metabolic Bone Diseases." Nuclear Medicine Seminars 8, no. 1 (April 15, 2022): 25–31. http://dx.doi.org/10.4274/nts.galenos.2022.0004.

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19

Allan, P. J., and S. Lal. "Metabolic bone diseases in intestinal failure." Journal of Human Nutrition and Dietetics 33, no. 3 (December 11, 2019): 423–30. http://dx.doi.org/10.1111/jhn.12726.

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20

Hannan, Fadil M., Paul J. Newey, Michael P. Whyte, and Rajesh V. Thakker. "Genetic approaches to metabolic bone diseases." British Journal of Clinical Pharmacology 85, no. 6 (November 28, 2018): 1147–60. http://dx.doi.org/10.1111/bcp.13803.

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21

Whyte, Michael P. "Heritable Metabolic and Dysplastic Bone Diseases." Endocrinology and Metabolism Clinics of North America 19, no. 1 (March 1990): 133–73. http://dx.doi.org/10.1016/s0889-8529(18)30342-6.

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22

Lipkin, Edward W. "METABOLIC BONE DISEASE IN GUT DISEASES." Gastroenterology Clinics of North America 27, no. 2 (June 1998): 513–23. http://dx.doi.org/10.1016/s0889-8553(05)70016-9.

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23

Parkman, Robertson, and Gay Crooks. "BONE MARROW TRANSPLANTATION FOR METABOLIC DISEASES." Immunology and Allergy Clinics of North America 16, no. 2 (May 1996): 429–38. http://dx.doi.org/10.1016/s0889-8561(05)70254-x.

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24

Wang, Yan, Fan Wu, and Yukun Li. "TRACP-5b and metabolic bone diseases." Bone 43 (October 2008): S91—S92. http://dx.doi.org/10.1016/j.bone.2008.07.124.

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25

Varlet, Alice-Anaïs, Emmanuèle Helfer, and Catherine Badens. "Molecular and Mechanobiological Pathways Related to the Physiopathology of FPLD2." Cells 9, no. 9 (August 23, 2020): 1947. http://dx.doi.org/10.3390/cells9091947.

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Laminopathies are rare and heterogeneous diseases affecting one to almost all tissues, as in Progeria, and sharing certain features such as metabolic disorders and a predisposition to atherosclerotic cardiovascular diseases. These two features are the main characteristics of the adipose tissue-specific laminopathy called familial partial lipodystrophy type 2 (FPLD2). The only gene that is involved in FPLD2 physiopathology is the LMNA gene, with at least 20 mutations that are considered pathogenic. LMNA encodes the type V intermediate filament lamin A/C, which is incorporated into the lamina meshwork lining the inner membrane of the nuclear envelope. Lamin A/C is involved in the regulation of cellular mechanical properties through the control of nuclear rigidity and deformability, gene modulation and chromatin organization. While recent studies have described new potential signaling pathways dependent on lamin A/C and associated with FPLD2 physiopathology, the whole picture of how the syndrome develops remains unknown. In this review, we summarize the signaling pathways involving lamin A/C that are associated with the progression of FPLD2. We also explore the links between alterations of the cellular mechanical properties and FPLD2 physiopathology. Finally, we introduce potential tools based on the exploration of cellular mechanical properties that could be redirected for FPLD2 diagnosis.

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26

Delgadillo-Velázquez, Jaime, Herminia Mendivil-Alvarado, Carlos Daniel Coronado-Alvarado, and Humberto Astiazaran-Garcia. "Extracellular Vesicles from Adipose Tissue Could Promote Metabolic Adaptation through PI3K/Akt/mTOR." Cells 11, no. 11 (June 3, 2022): 1831. http://dx.doi.org/10.3390/cells11111831.

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Extracellular vesicles (EVs) are nanoparticles secreted by cells under physiological and pathological conditions, such as metabolic diseases. In this context, EVs are considered potential key mediators in the physiopathology of obesity. It has been reported that EVs derived from adipose tissue (ADEVs) contribute to the development of a local inflammatory response that leads to adipose tissue dysfunction. In addition, it has been proposed that EVs are associated with the onset and progression of several obesity-related metabolic diseases such as insulin resistance. In particular, characterizing the molecular fingerprint of obesity-related ADEVs can provide a bigger picture that better reflects metabolic adaptation though PI3K/Akt/mTOR. Hence, in this review we describe the possible crosstalk communication of ADEVs with metabolically active organs and the intracellular response in the insulin signaling pathway.

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27

Mikosch, Peter. "Bone scintigraphy for the diagnosis of metabolic bone diseases." Wiener Medizinische Wochenschrift 154, no. 5-6 (March 2004): 119–26. http://dx.doi.org/10.1007/s10354-004-0053-4.

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28

Aggarwal, Juhi, Mansi Modi, RajNarayan Gupta, and EramHussain Pasha. "Utility of bone turnover markers in metabolic bone diseases." Santosh University Journal of Health Sciences 9, no. 1 (2023): 48. http://dx.doi.org/10.4103/sujhs.sujhs_38_23.

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29

Testini, Valentina, Laura Eusebi, Umberto Tupputi, Francesca Anna Carpagnano, Francesco Bartelli, and Giuseppe Guglielmi. "Metabolic Bone Diseases in the Pediatric Population." Seminars in Musculoskeletal Radiology 25, no. 01 (February 2021): 094–104. http://dx.doi.org/10.1055/s-0040-1722566.

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AbstractBone plays an important role in regulating mineral balance in response to physiologic needs. In addition, bone is subject to a continuous remodeling process to maintain healthy bone mass and growth. Metabolic bone diseases are a heterogeneous group of diseases caused by abnormalities of bone mass, mineral structure homeostasis, bone turnover, or bone growth. In pediatrics, several significant advances have been made in recent years in the diagnosis of metabolic bone diseases (e.g., osteogenesis imperfecta, hyperparathyroidism, rickets, renal osteodystrophy, pediatric osteoporosis, and osteopetrosis). Imaging is fundamental in the diagnosis of these pathologies.

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30

Zhang, Rubin. "Metabolic bone diseases in kidney transplant recipients." World Journal of Nephrology 1, no. 5 (2012): 127. http://dx.doi.org/10.5527/wjn.v1.i5.127.

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31

Moya-Angeler, Joaquin, Joseph M. Lane, and Jose A. Rodriguez. "Metabolic Bone Diseases and Total Hip Arthroplasty." Journal of the American Academy of Orthopaedic Surgeons 25, no. 11 (November 2017): 725–35. http://dx.doi.org/10.5435/jaaos-d-16-00067.

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32

Laxer, Eric B., and Max Aebi. "Metabolic bone diseases of the spinal column." Current Opinion in Orthopaedics 5, no. 2 (April 1994): 58–68. http://dx.doi.org/10.1097/00001433-199404000-00010.

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33

Wendlová, Jaroslava. "Metabolic bone diseases: basic and clinical aspects." Wiener Medizinische Wochenschrift 157, no. 23-24 (December 2007): 581. http://dx.doi.org/10.1007/s10354-007-0488-5.

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34

Hamdy, Neveen A. T. "Role of bisphosphonates in metabolic bone diseases." Trends in Endocrinology & Metabolism 4, no. 1 (January 1993): 19–25. http://dx.doi.org/10.1016/1043-2760(93)90059-n.

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35

Oton-Gonzalez, Lucia, Chiara Mazziotta, Maria Rosa Iaquinta, Elisa Mazzoni, Riccardo Nocini, Lorenzo Trevisiol, Antonio D’Agostino, Mauro Tognon, John Charles Rotondo, and Fernanda Martini. "Genetics and Epigenetics of Bone Remodeling and Metabolic Bone Diseases." International Journal of Molecular Sciences 23, no. 3 (January 28, 2022): 1500. http://dx.doi.org/10.3390/ijms23031500.

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Bone metabolism consists of a balance between bone formation and bone resorption, which is mediated by osteoblast and osteoclast activity, respectively. In order to ensure bone plasticity, the bone remodeling process needs to function properly. Mesenchymal stem cells differentiate into the osteoblast lineage by activating different signaling pathways, including transforming growth factor β (TGF-β)/bone morphogenic protein (BMP) and the Wingless/Int-1 (Wnt)/β-catenin pathways. Recent data indicate that bone remodeling processes are also epigenetically regulated by DNA methylation, histone post-translational modifications, and non-coding RNA expressions, such as micro-RNAs, long non-coding RNAs, and circular RNAs. Mutations and dysfunctions in pathways regulating the osteoblast differentiation might influence the bone remodeling process, ultimately leading to a large variety of metabolic bone diseases. In this review, we aim to summarize and describe the genetics and epigenetics of the bone remodeling process. Moreover, the current findings behind the genetics of metabolic bone diseases are also reported.

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36

Undale, Anita H., Jennifer J. Westendorf, Michael J. Yaszemski, and Sundeep Khosla. "Mesenchymal Stem Cells for Bone Repair and Metabolic Bone Diseases." Mayo Clinic Proceedings 84, no. 10 (October 2009): 893–902. http://dx.doi.org/10.4065/84.10.893.

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37

Torri, Francesca, Piervito Lopriore, Vincenzo Montano, Gabriele Siciliano, Michelangelo Mancuso, and Giulia Ricci. "Pathophysiology and Management of Fatigue in Neuromuscular Diseases." International Journal of Molecular Sciences 24, no. 5 (March 5, 2023): 5005. http://dx.doi.org/10.3390/ijms24055005.

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Fatigue is a major determinant of quality of life and motor function in patients affected by several neuromuscular diseases, each of them characterized by a peculiar physiopathology and the involvement of numerous interplaying factors. This narrative review aims to provide an overview on the pathophysiology of fatigue at a biochemical and molecular level with regard to muscular dystrophies, metabolic myopathies, and primary mitochondrial disorders with a focus on mitochondrial myopathies and spinal muscular atrophy, which, although fulfilling the definition of rare diseases, as a group represent a representative ensemble of neuromuscular disorders that the neurologist may encounter in clinical practice. The current use of clinical and instrumental tools for fatigue assessment, and their significance, is discussed. A summary of therapeutic approaches to address fatigue, encompassing pharmacological treatment and physical exercise, is also overviewed.

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38

Cook, Gary J. R., Gopinath Gnanasegaran, and Sue Chua. "Miscellaneous Indications in Bone Scintigraphy: Metabolic Bone Diseases and Malignant Bone Tumors." Seminars in Nuclear Medicine 40, no. 1 (January 2010): 52–61. http://dx.doi.org/10.1053/j.semnuclmed.2009.08.002.

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39

Bonora, Massimo, Simone Patergnani, Daniela Ramaccini, Giampaolo Morciano, Gaia Pedriali, Asrat Endrias Kahsay, Esmaa Bouhamida, Carlotta Giorgi, Mariusz R. Wieckowski, and Paolo Pinton. "Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology." Biomolecules 10, no. 7 (July 4, 2020): 998. http://dx.doi.org/10.3390/biom10070998.

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Mitochondrial permeability transition (MPT) is the sudden loss in the permeability of the inner mitochondrial membrane (IMM) to low-molecular-weight solutes. Due to osmotic forces, MPT is paralleled by a massive influx of water into the mitochondrial matrix, eventually leading to the structural collapse of the organelle. Thus, MPT can initiate outer-mitochondrial-membrane permeabilization (MOMP), promoting the activation of the apoptotic caspase cascade and caspase-independent cell-death mechanisms. The induction of MPT is mostly dependent on mitochondrial reactive oxygen species (ROS) and Ca2+, but is also dependent on the metabolic stage of the affected cell and signaling events. Therefore, since its discovery in the late 1970s, the role of MPT in human pathology has been heavily investigated. Here, we summarize the most significant findings corroborating a role for MPT in the etiology of a spectrum of human diseases, including diseases characterized by acute or chronic loss of adult cells and those characterized by neoplastic initiation.

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40

Rey-Reñones, Cristina, Jose Miguel Baena-Díez, Isabel Aguilar-Palacio, Cristina Miquel, and María Grau. "Type 2 Diabetes Mellitus and Cancer: Epidemiology, Physiopathology and Prevention." Biomedicines 9, no. 10 (October 9, 2021): 1429. http://dx.doi.org/10.3390/biomedicines9101429.

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Individuals with type 2 diabetes mellitus are at greater risk of developing cancer and of dying from it. Both diseases are age-related, contributing to the impact of population aging on the long-term sustainability of health care systems in European Union countries. The purpose of this narrative review was to describe, from epidemiological, pathophysiological and preventive perspectives, the links between type 2 diabetes mellitus and the most prevalent cancers in these patients. Multiple metabolic abnormalities that may occur in type 2 diabetes mellitus, particularly obesity, could explain the increased cancer risk. In addition, the effectiveness of drugs commonly used to treat type 2 diabetes mellitus (e.g., metformin and thiazolidinediones) has been broadly evaluated in cancer prevention. Thus, a better understanding of the links between type 2 diabetes mellitus and cancer will help to identify the contributing factors and the pathophysiological pathways and to design personalized preventive strategies. The final goal is to facilitate healthy aging and the prevention of cancer and other diseases related with type 2 diabetes mellitus, which are among the main sources of disability and death in the European Union and worldwide.

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41

Shiraki, M. "Recent advances in metabolic bone diseases of the elderly. Calcium requirement and bone metabolic marker." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 29, no. 2 (1992): 101–4. http://dx.doi.org/10.3143/geriatrics.29.101.

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42

Cordani, Marco, Miguel Sánchez-Álvarez, Raffaele Strippoli, Alexandr V. Bazhin, and Massimo Donadelli. "Sestrins at the Interface of ROS Control and Autophagy Regulation in Health and Disease." Oxidative Medicine and Cellular Longevity 2019 (May 7, 2019): 1–11. http://dx.doi.org/10.1155/2019/1283075.

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Reactive oxygen species (ROS) and autophagy are two highly complex and interrelated components of cell physiopathology, but our understanding of their integration and their contribution to cell homeostasis and disease is still limited. Sestrins (SESNs) belong to a family of highly conserved stress-inducible proteins that orchestrate antioxidant and autophagy-regulating functions protecting cells from various noxious stimuli, including DNA damage, oxidative stress, hypoxia, and metabolic stress. They are also relevant modulators of metabolism as positive regulators of the key energy sensor AMP-dependent protein kinase (AMPK) and inhibitors of mammalian target of rapamycin complex 1 (mTORC1). Since perturbations in these pathways are central to multiple disorders, SESNs might constitute potential novel therapeutic targets of broad interest. In this review, we discuss the current understanding of regulatory and effector networks of SESNs, highlighting their significance as potential biomarkers and therapeutic targets for different diseases, such as aging-related diseases, metabolic disorders, neurodegenerative diseases, and cancer.

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43

Zhu, Mei, and Mingcai Qiu. "Bone biopsy in various metabolic bone diseases studied by bone histomorphometry in China." Journal of Bone and Mineral Metabolism 23, S1 (January 2005): 69–75. http://dx.doi.org/10.1007/bf03026326.

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44

STEVENS, A., and JANET PALMER. "Frozen sections of bone biopsies in metabolic and other bone diseases." Histopathology 9, no. 3 (March 1985): 315–24. http://dx.doi.org/10.1111/j.1365-2559.1985.tb02449.x.

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45

Ballanti, P., C. Della Rocca, E. Bonucci, S. Milani, V. Lo Cascio, and B. Imbimbo. "Sensitivity of Bone Histomorphometry in the Diagnosis of Metabolic Bone Diseases." Pathology - Research and Practice 185, no. 5 (December 1989): 786–89. http://dx.doi.org/10.1016/s0344-0338(89)80240-7.

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Cho, Tae Joon, Min Bum Kim, In Ho Choi, Chin Youb Chung, Won Joon Yoo, and Choon Ki Lee. "Orthopedic Treatments for Genetic and Metabolic Bone Diseases." Journal of the Korean Orthopaedic Association 38, no. 4 (2003): 378. http://dx.doi.org/10.4055/jkoa.2003.38.4.378.

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Suzuki, Yasuo. "5. Biomarkers in Diagnosis of Metabolic Bone Diseases." Nihon Naika Gakkai Zasshi 96, no. 10 (2007): 2151–58. http://dx.doi.org/10.2169/naika.96.2151.

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Arantes, Henrique Pierotti, André Gonçalves da Silva, and Marise Lazaretti-Castro. "Bisphosphonates in the treatment of metabolic bone diseases." Arquivos Brasileiros de Endocrinologia & Metabologia 54, no. 2 (March 2010): 206–12. http://dx.doi.org/10.1590/s0004-27302010000200017.

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Abstract:

Osteoporosis is a disease characterized by low bone mass associated with the deterioration of microarchitecture, due to an imbalance either in high bone resorption or low bone formation or in both, leading to a high risk of fractures. Bisphosphonates are medications which reduce the ability of osteoclasts to induce bone resorption and consequently improve the balance between resorption and formation. There are bisphosphonates approved for the prevention and treatment of osteoporosis. Administration can be oral (daily, weekly or monthly) or intravenous (quarterly or yearly). These medications are well tolerated and with the correct instructions of administration have a good safety profile. Serious side effects, such as, osteonecrosis of jaw is very rare. Bisphosphonates are the most prescribed medication for the treatment of osteoporosis.

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Drake, Matthew T., Serge Cremers, R. Graham Russell, and John P. Bilezikian. "Drugs for the treatment of metabolic bone diseases." British Journal of Clinical Pharmacology 85, no. 6 (April 4, 2019): 1049–51. http://dx.doi.org/10.1111/bcp.13857.

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Riggs, Matthew M., and Serge Cremers. "Pharmacometrics and systems pharmacology for metabolic bone diseases." British Journal of Clinical Pharmacology 85, no. 6 (February 28, 2019): 1136–46. http://dx.doi.org/10.1111/bcp.13881.

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