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      Heshouwu ( Polygonum multiflorum Thunb.) Extract Attenuates Bone Loss in Diabetic Mice

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          Abstract

          This study investigated the effects and mechanism of Heshouwu ( Polygonum multiflorum Thunb.) water extract (HSW) on diabetes-related bone loss in mice. HSW was orally administered (300 mg/kg body weight) to high-fat diet and streptozotocin-induced diabetic mice for 10 weeks. HSW significantly alleviated mouse body weight loss and hyperglycemia compared with the control group, and elevated serum levels of insulin, osteocalcin, and bone-alkaline phosphatase. HSW supplementation also significantly increased the bone volume/tissue volume ratio and trabecular thickness and number, and decreased the bone surface/bone volume ratio and trabecular structure model index in the femur and tibia. Moreover, HSW significantly increased femoral bone mineral density. In addition, HSW down-regulated osteoclastogenic genes, such as nuclear factor of activated T-cells, cytoplasmic 1 and tartrate-resistant acid phosphatase 5 ( TRAP), in both the femur and tibia tissue, and reduced serum TRAP level compare to those of control mice. These results indicate that HSW might relieve diabetes-related bone disorders through regulating osteoclast-related genes, suggesting HSW may be used as a preventive agent for diabetes-induced bone loss.

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          Regulation of NFATc1 in Osteoclast Differentiation

          Jung Kim, Nacksung Kim (2014)
          Osteoclasts are unique cells that degrade the bone matrix. These large multinucleated cells differentiate from the monocyte/macrophage lineage upon stimulation by two essential cytokines, macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL). Activation of transcription factors such as microphthalmia transcription factor (MITF), c-Fos, NF-κB, and nuclear factor-activated T cells c1 (NFATc1) is required for sufficient osteoclast differentiation. In particular, NFATc1 plays the role of a master transcription regulator of osteoclast differentiation. To date, several mechanisms, including transcription, methylation, ubiquitination, acetylation, and non-coding RNAs, have been shown to regulate expression and activation of NFATc1. In this review, we have summarized the various mechanisms that control NFATc1 regulation during osteoclast differentiation.
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            Mechanisms of Bone Resorption in Periodontitis

            Stefan A. Hienz, Sweta Paliwal, Saso Ivanovski (2015)
            Alveolar bone loss is a hallmark of periodontitis progression and its prevention is a key clinical challenge in periodontal disease treatment. Bone destruction is mediated by the host immune and inflammatory response to the microbial challenge. However, the mechanisms by which the local immune response against periodontopathic bacteria disturbs the homeostatic balance of bone formation and resorption in favour of bone loss remain to be established. The osteoclast, the principal bone resorptive cell, differentiates from monocyte/macrophage precursors under the regulation of the critical cytokines macrophage colony-stimulating factor, RANK ligand, and osteoprotegerin. TNF-α, IL-1, and PGE2 also promote osteoclast activity, particularly in states of inflammatory osteolysis such as those found in periodontitis. The pathogenic processes of destructive inflammatory periodontal diseases are instigated by subgingival plaque microflora and factors such as lipopolysaccharides derived from specific pathogens. These are propagated by host inflammatory and immune cell influences, and the activation of T and B cells initiates the adaptive immune response via regulation of the Th1-Th2-Th17 regulatory axis. In summary, Th1-type T lymphocytes, B cell macrophages, and neutrophils promote bone loss through upregulated production of proinflammatory mediators and activation of the RANK-L expression pathways.
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              The impact of diabetes and diabetes medications on bone health.

              Matthew P Gilbert, Richard Pratley (2015)
              Patients with type 2 diabetes mellitus (T2DM) have an increased risk of fragility fractures despite increased body weight and normal or higher bone mineral density. The mechanisms by which T2DM increases skeletal fragility are unclear. It is likely that a combination of factors, including a greater risk of falling, regional osteopenia, and impaired bone quality, contributes to the increased fracture risk. Drugs for the treatment of T2DM may also impact on the risk for fractures. For example, thiazolidinediones accelerate bone loss and increase the risk of fractures, particularly in older women. In contrast, metformin and sulfonylureas do not appear to have a negative effect on bone health and may, in fact, protect against fragility fracture. Animal models indicate a potential role for incretin hormones in bone metabolism, but there are only limited data on the impact of dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 agonists on bone health in humans. Animal models also have demonstrated a role for amylin in bone metabolism, but clinical trials in patients with type 1 diabetes with an amylin analog (pramlintide) have not shown a significant impact on bone metabolism. The effects of insulin treatment on fracture risk are inconsistent with some studies showing an increased risk and others showing no effect. Finally, although there is limited information on the latest class of medications for the treatment of T2DM, the sodium-glucose co-transporter-2 inhibitors, these drugs do not seem to increase fracture risk. Because diabetes is an increasingly common chronic condition that can affect patients for many decades, further research into the effects of agents for the treatment of T2DM on bone metabolism is warranted. In this review, the physiological mechanisms and clinical impact of diabetes treatments on bone health and fracture risk in patients with T2DM are described.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Prev Nutr Food Sci
                Journal ID (iso-abbrev): Prev Nutr Food Sci
                Title: Preventive Nutrition and Food Science
                Publisher: The Korean Society of Food Science and Nutrition
                ISSN (Print): 2287-1098
                ISSN (Electronic): 2287-8602
                Publication date (Print): June 2019
                Publication date (Electronic): 30 June 2019
                Volume: 24
                Issue: 2
                Pages: 121-127
                Affiliations
                [1 ]Department of Food and Nutrition, Sunchon National University, Jeonnam 57922, Korea
                [2 ]Mokpo Marin Food-Industry Research Center, Jeonnam 58621, Korea
                [3 ]Suncheon Research Center for Natural Medicines, Jeonnam 57922, Korea
                [4 ]College of Pharmacy, Sunchon National University, Jeonnam 57922, Korea
                Author notes
                Correspondence to Mi-Kyung Lee, Tel: +82-61-750-3656, E-mail: leemk@ 123456scnu.ac.kr

                Author information: Ju Ri Ham (Graduate Student), Ra-Yeong Choi (Graduate Student), Hyo-Seon Ryu (Graduate Student), Sung-Tae Yee (Professor), Mi-Kyung Lee (Professor)

                Article
                Publisher ID: pnfs-24-121
                DOI: 10.3746/pnf.2019.24.2.121
                PMC ID: 6615354
                SO-VID: 11a67aa8-916c-4f40-9c69-8568a35ede2a
                Copyright © Copyright © 2019 by The Korean Society of Food Science and Nutrition
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 11 February 2019
                Date accepted : 12 March 2019
                Categories
                Subject: Articles

                Keywords: bone microarchitecture,diabetes,heshouwu,polygonum multiflorum thunb.,osteoporosis
                Data availability:
                Keywords: bone microarchitecture, diabetes, heshouwu, polygonum multiflorum thunb., osteoporosis

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