骨ルポ
ASBMR 2022 レポート
LIU TAO（東京医科歯科大学整形外科）
This is my first time to attend a large international academic conference like ASBMR and I feel very honored and excited. Especially, my poster won the travel award, which is very appreciated for a new researcher like me. I was very excited to be able to participate in a large international conference like ASBMR. Throughout the conference, I worked hard to capture new information and also increased my knowledge. I look forward to attending such international conferences in the future and presenting our research there as well.
紹介演題 [1]
Sirt3 mediates the benefits of exercise on bone in aged mice
キーワード
Sirt3, aging, Osteoporosis
研究グループ
Qiangqiang Li[1], Jack Chun-yiu Cheng[2], Qing Jiang[1], Wayne Yuk-wai Lee[2].
- [1] Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, China
- [2] Department of Orthopaedics and Traumatology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong
サマリー＆コメント
Osteocytes are the major bone cells responsible for transforming mechanical stimuli into cellular signals through their highly specialized lacunocanalicular networks (LCN). Osteocyte LCN degenerate with aging, thus might impair the effectiveness of exercise on bone health; however, the underlying mechanism and clinical implications remain elusive. Sirt3 is critical for mitochondrial biogenesis and declined Sirt3 expression has been implicated in some age-related disorders. Being the longest living bone cells, we hypothesized that osteocytes are vulnerable to the change of Sirt3 expression with aging and the reduced Sirt3 expression in osteocytes would debilitate benefits of exercise on bone health in aged mice. The declined Sirt3 expression in osteocytes could be one of the factors underlying poor response to exercise in aged bone. Targeting Sirt3 could be a novel therapeutic strategy to prevent age-related bone loss and augment the benefits of exercise in the elderly.
For me, this topic is very interesting because it is related to my research area. I am currently doing research related to Sirt6. Now I am considering to use this valuable new discovery to propose some different hypotheses for future research.
紹介演題 [2]
Emerging role of FGF23 in the regulation of metabolic homeostasis
キーワード
FGF23, body fat mass and abdominal obesity
研究グループ
Min Young Park[1], Chia-Ling Tu[2], Wenhan Chang[2], Despina Sitara[1].
- [1] New York University, United States
- [2] San Francisco VA Medical Center, UCSF, United States
サマリー＆コメント
Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that regulates phosphate homeostasis and vitamin D metabolism. In addition to its central role in mineral balance, recent findings suggested that FGF23 is associated with chronic metabolic conditions including cardiovascular disease, diabetes mellitus, and obesity. Circulating FGF23 levels are elevated in obese individuals, and they are correlated with body fat mass and abdominal obesity. Moreover, consumption of high fat diet (HFD) increases serum FGF23 levels. However, the actions of FGF23 in adipocytes and its role in lipid metabolism have not been demonstrated. To understand the role of FGF23 in adipocytes, particularly in obesity, we generated adipocyte-specific Fgf23 null mice using Cre recombinase under the control of the mouse adiponectin (Adipoq) promoter. Both male and female control (Fgf23flox/flox) and knockout (KO, AdipoqFgf23flox/flox) mice were fed either HFD (60 %kcal fat) or normal fat diet (NFD) at 8 weeks of age for 24 weeks. Body weight measurements were taken every week and percentage of body fat was determined longitudinally during 24 weeks of diet intervention by an EchoMRI scanner. Serum, adipose tissue, and liver were collected upon sacrifice. After 24 weeks of HFD, male control and KO mice had comparable gain in body weight (BW) and body fat percentage. However, female KO mice had significantly lower body weight and percentage of body fat. Moreover, serum total cholesterol levels were reduced in female KO mice. Triglyceride (TG) content in the liver was significantly reduced in female KO mice, and it corresponded with downregulation of lipid droplet protein Perilipin and fatty acid transporter CD36 mRNA expression in the liver. Transcript levels of hepatic PPARγ, which is positively correlated with fat accumulation in obesity, were also suppressed in female KO mice compared to controls. Obesity is associated with low-grade chronic inflammation, and we found that hepatic mRNA expression of the inflammatory cytokine TNFα was diminished in female KO mice, suggesting that adipocytic Fgf23 modulates lipid accumulation and inflammation. In summary, our results demonstrate for the first time that adipocyte-specific ablation of Fgf23 alleviates diet-induced obesity and regulates lipid metabolism in a sex-specific manner.
This direction of research on FGF23 is something I have not covered before. This is because I have previously been studying the changes in FGF23 during phosphorus metabolism for bone mass in mice. This article starts from the adipocyte aspect and reveals that FGF23 regulates lipid accumulation and inflammation. With this article, I can expand the direction of my research and provide different ideas for my experiments.