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      Molecular Modulation of Osteoblasts and Osteoclasts in Type 2 Diabetes

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      Author(s): 1 , 1 , 1 , 2 ,
      Publication date (Electronic):
      Journal: Journal of Diabetes Research
      Publisher: Hindawi

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          Abstract

          Diabetes is a common disease affecting majority of populations worldwide. Since 1980, there has been an increase in the number of people diagnosed as prediabetic and diabetic. Diabetes is characterized by high levels of circulating glucose and leads to most microvascular and macrovascular complications such as retinopathy, nephropathy, neuropathy, stroke, and myocardial infarction. Bone marrow vascular disruption and increased adiposity are also linked to various complications in type II diabetes mellitus. In addition to these complications, type 2 diabetic patients also have fragile bones caused by faulty mineralization mainly due to increased adiposity among diabetic patients that affects both osteoblast and osteoclast functions. Other factors that increase fracture risk in diabetic patients are increased oxidative stress, inflammation, and drugs administered to diabetic patients. This review reports the modulation of different pathways that affect bone metabolism in diabetic conditions.

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          Systematic review of type 1 and type 2 diabetes mellitus and risk of fracture.

          Mohsen Janghorbani, Rob Van Dam, Walter C. Willett … (2007)
          The authors conducted a systematic review of published data on the association between diabetes mellitus and fracture. The authors searched MEDLINE through June 2006 and examined the reference lists of pertinent articles (limited to studies in humans). Summary relative risks and 95% confidence intervals were calculated with a random-effects model. The 16 eligible studies (two case-control studies and 14 cohort studies) included 836,941 participants and 139,531 incident cases of fracture. Type 2 diabetes was associated with an increased risk of hip fracture in both men (summary relative risk (RR) = 2.8, 95% confidence interval (CI): 1.2, 6.6) and women (summary RR = 2.1, 95% CI: 1.6, 2.7). Results were consistent between studies of men and women and between studies conducted in the United States and Europe. The association between type of diabetes and hip fracture incidence was stronger for type 1 diabetes (summary RR = 6.3, 95% CI: 2.6, 15.1) than for type 2 diabetes (summary RR = 1.7, 95% CI: 1.3, 2.2). Type 2 diabetes was weakly associated with fractures at other sites, and most effect estimates were not statistically significant. These findings strongly support an association between both type 1 and type 2 diabetes and increased risk of hip fracture in men and women.
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            Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.

            P Ducy, M Amling, S. Takeda … (2000)
            Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.
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              The evolution of Fox genes and their role in development and disease.

              Sridhar Hannenhalli, Klaus Kaestner (2009)
              The forkhead box (Fox) family of transcription factors, which originated in unicellular eukaryotes, has expanded over time through multiple duplication events, and sometimes through gene loss, to over 40 members in mammals. Fox genes have evolved to acquire a specialized function in many key biological processes. Mutations in Fox genes have a profound effect on human disease, causing phenotypes as varied as cancer, glaucoma and language disorders. We summarize the salient features of the evolution of the Fox gene family and highlight the diverse contribution of various Fox subfamilies to developmental processes, from organogenesis to speech acquisition.
              Article 0 comments Cited 241 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jameela Banu:
                ORCID: http://orcid.org/0000-0003-4034-7204
                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date Collection: 2018
                Publication date (Electronic): 4 November 2018
                Volume: 2018
                Electronic Location Identifier: 6354787
                Affiliations
                1Department of Health and Biomedical Sciences, College of Health Affairs, University of Texas Rio Grande Valley, 1201, W University Dr, Edinburg, TX 78539, USA
                2Department of Biology, College of Sciences, University of Texas Rio Grande Valley, 1201, W University Dr, Edinburg, TX 78539, USA
                Author notes

                Academic Editor: Hiroshi Okamoto

                Author information
                http://orcid.org/0000-0003-4034-7204
                Article
                DOI: 10.1155/2018/6354787
                PMC ID: 6247387
                PubMed ID: 30525054
                SO-VID: c3d04d3a-9a22-4ff3-a418-fc254815ae92
                Copyright © Copyright © 2018 Selvalakshmi Rathinavelu et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 3 April 2018
                Date revision received : 16 July 2018
                Date accepted : 14 August 2018
                Categories
                Subject: Review Article

                Data availability:

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