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      Fat, adipokines, bone structure and bone regulatory factors associations in obesity

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          Abstract

          Context

          Obese (OB) adults (BMI ≥ 30) have a higher bone mineral density (BMD) and more favourable bone microarchitecture than normal-weight (NW) adults (BMI 18.5–24.9).

          Objective

          The objective of this study was to identify which fat compartments have the strongest association with bone density and bone turnover and whether biochemical factors (adipokines, hormones and bone regulators) are likely to be important mediators of the effect of obesity on bone.

          Design

          This was a cross-sectional, observational, matched case-control study.

          Setting

          Participants were recruited from the local community.

          Participants

          Two hundred healthy men and women aged 25–40 or 55–75 were recruited in individually matched OB and NW pairs. Body composition, BMD and bone microarchitecture were determined by dual-energy X-ray absorptiometry (DXA), computed tomography (CT) and high-resolution peripheral CT (HR-pQCT). Bone turnover and potential regulators such as C-terminal cross-linking telopeptide (CTX), type 1 procollagen N-terminal peptide (PINP), sclerostin, periostin, parathyroid hormone (PTH), 25-hydroxyvitamin D (25OHD), insulin-like growth factor 1 (IGF1), adiponectin, leptin and insulin were assessed.

          Main outcome

          Planned exploratory analysis of the relationships between fat compartments, areal and volumetric BMD, bone microarchitecture, bone turnover markers and bone regulators.

          Results

          Compared with NW, OB had lower CTX, PINP, adiponectin, IGF1, and 25OHD and higher leptin, PTH and insulin (all P < 0.05). CTX and subcutaneous adipose tissue (SAT) were the bone marker and fat compartment most consistently associated with areal and volumetric BMD. In regression models, SAT was negatively associated with CTX ( P < 0.001). When leptin was added to the model, SAT was no longer associated with CTX, but leptin ( P < 0.05) was negatively associated with CTX.

          Conclusions

          SAT is associated with lower bone resorption and properties favourable for bone strength in obesity. Leptin may be an important mediator of the effects of SAT on the skeleton.

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          Most cited references29

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          Subcutaneous and visceral adipose tissue: structural and functional differences.

          Obesity is a heterogeneous disorder. Obese individuals vary in their body fat distribution, their metabolic profile and degree of associated cardiovascular and metabolic risk. Abdominal obesity carries greater risk of developing diabetes and future cardiovascular events than peripheral or gluteofemoral obesity. There are differences between adipose tissue present in subcutaneous areas (SCAT) and visceral adipose tissue (VAT) present in the abdominal cavity. These include anatomical, cellular, molecular, physiological, clinical and prognostic differences. Anatomically, VAT is present mainly in the mesentery and omentum, and drains directly through the portal circulaion to the liver. VAT compared with SCAT is more cellular, vascular, innervated and contains a larger number of inflammatory and immune cells, lesser preadipocyte differentiating capacity and a greater percentage of large adipocytes. There are more glucocorticoid and androgen receptors in VAT than in SCAT. VAT adipocytes are more metabolically active, more sensitive to lipolysis and more insulin-resistant than SCAT adipocytes. VAT has a greater capacity to generate free fatty acids and to uptake glucose than SCAT and is more sensitive to adrenergic stimulation, while SCAT is more avid in absorption of circulating free fatty acids and triglycerides. VAT carries a greater prediction of mortality than SCAT.
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            Guidelines for the assessment of bone density and microarchitecture in vivo using high-resolution peripheral quantitative computed tomography

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              Identification and characterization of a novel protein, periostin, with restricted expression to periosteum and periodontal ligament and increased expression by transforming growth factor beta.

              We had previously identified the cDNA for a novel protein called osteoblast-specific factor 2 (OSF-2) from an MC3T3-E1 cDNA library using subtraction hybridization and differential screening techniques. Here we describe the localization, regulation, and potential function of this protein. Immunohistochemistry using specific antiserum revealed that in adult mice, the protein is preferentially expressed in periosteum and periodontal ligament, indicating its tissue specificity and a potential role in bone and tooth formation and maintenance of structure. Based on this observation and the fact that other proteins have been called OSF-2, the protein was renamed "periostin." Western blot analysis showed that periostin is a disulfide linked 90 kDa protein secreted by osteoblasts and osteoblast-like cell lines. Nucleotide sequence revealed four periostin transcripts that differ in the length of the C-terminal domain, possibly caused by alternative splicing events. Reverse transcription- polymerase chain reaction analysis revealed that these isoforms are not expressed uniformly but are differentially expressed in various cell lines. Both purified periostin protein and the periostin-Fc recombinant protein supported attachment and spreading of MC3T3-E1 cells, and this effect was impaired by antiperiostin antiserum, suggesting that periostin is involved in cell adhesion. The protein is highly homologous to betaig-h3, a molecule induced by transforming growth factor beta (TGF-beta) that promotes the adhesion and spreading of fibroblasts. Because TGF-beta has dramatic effects on periosteal expansion and the recruitment of osteoblast precursors, this factor was tested for its effects on periostin expression. By Western blot analysis, TGF-beta increased periostin expression in primary osteoblast cells. Together, these data suggest that periostin may play a role in the recruitment and attachment of osteoblast precursors in the periosteum.
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                Author and article information

                Journal
                Eur J Endocrinol
                Eur J Endocrinol
                EJE
                European Journal of Endocrinology
                Bioscientifica Ltd (Bristol )
                0804-4643
                1479-683X
                29 September 2022
                01 December 2022
                : 187
                : 6
                : 743-750
                Affiliations
                [1 ]Mellanby Centre for Bone Research , Department of Oncology and Metabolism, University of Sheffield, Sheffield, UK
                Author notes
                Correspondence should be addressed to T Vilaca; Email: T.vilaca@ 123456sheffield.ac.uk

                *(T Vilaca and A Evans contributed equally to this work)

                Author information
                http://orcid.org/0000-0002-9227-6076
                Article
                EJE-22-0530
                10.1530/EJE-22-0530
                9641785
                36173650
                a5fb2cd4-1704-4d57-b6c6-63c1bc9f13f4
                © The authors

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 14 June 2022
                : 29 September 2022
                Categories
                Original Research

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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