Special Issue "Effects of Type II Diabetes and Metabolic Disease on Bone and Muscle Health"

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (20 October 2021).

Special Issue Editors

Dr. Tara Clare Brennan-Speranza
E-Mail Website
Guest Editor
1. School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, Australia
2. School of Public Health, Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Interests: bone energy metabolism; osteoporosis; bone biology; bone mineral density
Dr. Christian M. Girgis
E-Mail Website
Guest Editor
1. Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, Australia
2. Department of Endocrinology, Royal North Shore Hospital, Sydney, Australia
3. Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Interests: obesity; diabetes ; cardiovascular disease; endocrinology; calcium; vitamin D; osteoporosis; sarcopenia; human nutrition; metabolism

Special Issue Information

Dear Colleagues,

The World Health Organization estimated that more than 422 million people worldwide had diabetes in 2014, which rose from around 108 million in 1980. The International Diabetes Foundation has predicted this number to increase to over 590 million by 2035. Increased musculoskeletal fragility, including diabetic sarcopenia and high fracture risk, are under-recognized complications of diabetes.

As a result, patients have a markedly higher incidence of falls and a large increase in overall fracture risk compared to the general population. The increase in fractures in patients with diabetes is independent of factors such as age, sex, BMI, visual impairment and even tendency to fall. This implies that the increased fracture risk is driven by compromised bone and muscle quality, although the exact mechanisms remain unclear and no standardized treatment or long-term public health strategies for improving musculoskeletal outcomes in these patients are available.

Preliminary evidence already indicates that the alarming decline in the age of onset of this epidemic disease is going to have even greater negative effects on the quality of bone and muscle and, most devastatingly, the resistance to fracture in younger people, considering exposure to the disease before peak bone and muscle mass is reached.

This Special Issue entitled “Effects of Type II Diabetes and Metabolic Disease on Bone and Muscle Health” aims to collect high-quality and up-to-date original and review articles regarding the multifactorial effects of hyperglycemia, insulin resistance, inflammation and other metabolic pathologies, as well as possible treatment options, on the musculoskeletal complications associated with these diseases.

Dr. Tara Clare Brennan-Speranza
Dr. Christian M. Girgis
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Type 2 diabetes and bone
  • Type 2 diabetes and muscle
  • Metabolic disease and bone microarchitecture
  • Bone turnover markers
  • Fracture risk

Published Papers (1 paper)

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Research

Article
Distinct Effects of a High Fat Diet on Bone in Skeletally Mature and Developing Male C57BL/6J Mice
Nutrients 2021, 13(5), 1666; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051666 - 14 May 2021
Cited by 3 | Viewed by 986
Abstract
Increased risks of skeletal fractures are common in patients with impaired glucose handling and type 2 diabetes mellitus (T2DM). The pathogenesis of skeletal fragility in these patients remains ill-defined as patients present with normal to high bone mineral density. With increasing cases of [...] Read more.
Increased risks of skeletal fractures are common in patients with impaired glucose handling and type 2 diabetes mellitus (T2DM). The pathogenesis of skeletal fragility in these patients remains ill-defined as patients present with normal to high bone mineral density. With increasing cases of glucose intolerance and T2DM it is imperative that we develop an accurate rodent model for further investigation. We hypothesized that a high fat diet (60%) administered to developing male C57BL/6J mice that had not reached skeletal maturity would over represent bone microarchitectural implications, and that skeletally mature mice would better represent adult-onset glucose intolerance and the pre-diabetes phenotype. Two groups of developing (8 week) and mature (12 week) male C57BL/6J mice were placed onto either a normal chow (NC) or high fat diet (HFD) for 10 weeks. Oral glucose tolerance tests were performed throughout the study period. Long bones were excised and analysed for ex vivo biomechanical testing, micro-computed tomography, 2D histomorphometry and gene/protein expression analyses. The HFD increased fasting blood glucose and significantly reduced glucose tolerance in both age groups by week 7 of the diets. The HFD reduced biomechanical strength, both cortical and trabecular indices in the developing mice, but only affected cortical outcomes in the mature mice. Similar results were reflected in the 2D histomorphometry. Tibial gene expression revealed decreased bone formation in the HFD mice of both age groups, i.e., decreased osteocalcin expression and increased sclerostin RNA expression. In the mature mice only, while the HFD led to a non-significant reduction in runt-related transcription factor 2 (Runx2) RNA expression, this decrease became significant at the protein level in the femora. Our mature HFD mouse model more accurately represents late-onset impaired glucose tolerance/pre-T2DM cases in humans and can be used to uncover potential insights into reduced bone formation as a mechanism of skeletal fragility in these patients. Full article
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