Osteocytes and Diabetes: Altered Function of Diabetic Osteocytes
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OSTEOCYTES (J DELGADO-CALLE AND J KLEIN-NULEND, SECTION EDITORS)
Osteocytes and Diabetes: Altered Function of Diabetic Osteocytes Arancha R. Gortázar 1,2
&
Juan A. Ardura 1,2
Accepted: 28 October 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Diabetes mellitus is a prevalent chronic disease affecting millions of people in the world. Bone fragility is a complication found in diabetic patients. Although osteoblasts and osteoclasts are directly affected by diabetes, herein we focus on how the diabetic state—based on hyperglycemia and accumulation of advanced glycation end products among other features— impairs osteocyte functions exerting deleterious effects on bone. Recent Findings In the last years, several studies described that diabetic conditions cause morphological modifications on lacunar-canalicular system, alterations on osteocyte mechanoreceptors and intracellular pathways and on osteocyte communication with other cells through the secretion of proteins such as sclerostin or RANKL. Summary This article gives an overview of events occurring in diabetic osteocytes. In particular, mechanical responses seem to be seriously affected in these conditions, suggesting that mechanical sensibility could be a target for future research in the field. Keywords Diabetes . Osteocytes . Hyperglycemia . Mechanoreceptors
Introduction Diabetes mellitus (DM) is a chronic metabolic disease with a high prevalence worldwide characterized by elevated levels of glucose in blood. Type 1 DM or insulin-dependent diabetes is caused by autoimmune destruction of insulin-producing βpancreatic cells and is usually developed during childhood. In contrast, type 2 DM, the most prevalent DM, is characterized by cell resistance to insulin and mainly affects adults. In addition to well-known renal and cardiovascular complications, an increased risk of bone fracture is reported in diabetic patients [1, 2]. However, the bone phenotype found in both types of diabetes is different. Whereas type I DM patients present a low bone mineral density (BMD), type 2 DM is associated with normal or even high BMD. High glucose This article is part of the Topical Collection on Osteocytes * Arancha R. Gortázar [email protected] 1
Bone Physiopathology laboratory, Applied Molecular Medicine Institute (IMMA), Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925 Alcorcón, Madrid, Spain
2
Departamento de Ciencias Médicas Básicas, Facultad de Medicina, Universidad San Pablo-CEU,CEU Universities, Campus Monteprincipe, 28925 Alcorcón, Madrid, Spain
(HG) concentration, oxidative stress and accumulation of advanced glycation end products (AGE) seem to be behind the deleterious effects on bone metabolism in diabetes. Thus, the diabetic state induces severe effects on bone cells including inhibition of proliferation and differentiation of mesenchymal cells, decrease in osteoblastic mineralisation and increase in osteoclast activity [3–5]. However, less known are the diabetic effects on osteocyt
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