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Nishimura Yuki Last modified date：2024.04.22

Assistant Professor / Section of Periodontology, Dividion of Oral Rehabilitation
Department of Dental Science
Faculty of Dental Science


Graduate School
Department of Dental Science
Graduate School of Dental Science
Undergraduate School
Department of Dentistry
School of Dentistry


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Homepage
https://kyushu-u.elsevierpure.com/en/persons/yuki-nishimura
　Reseacher Profiling Tool　Kyushu University Pure
Phone
092-642-6358
Fax
092-642-6360
Academic Degree
Doctor of Dentistry, Ph.D.
Country of degree conferring institution (Overseas)
No
Field of Specialization
Periodontology
Total Priod of education and research career in the foreign country
00years00months
Research
Research Interests
  • Verification of protection of pancreatic β-cell and prevention of diabetic periodontitis by gingival mesenchymal stem cell-derived exosomes
    keyword : pancreatic β-cell
    2022.04.
Academic Activities
Reports
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1. Iwashita M, Hayashi M, Nishimura Y, Yamashita A, The Link Between Periodontal Inflammation and Obesity., Current Oral Health Reports, 10.1007/s40496-021-00296-4, 2021.10.
Papers
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1. Yuki Nishimura, Misaki Iwashita, Masato Hayashi, Takanori Shinjo, Yukari Watanabe, Tatsuro Zeze, Akiko Yamashita, Takao Fukuda, Terukazu Sanui, Tomomi Sano, Tomoichiro Asano, Fusanori Nishimura, XAF1 overexpression exacerbates diabetes by promoting pancreatic beta-cell apoptosis, ACTA DIABETOLOGICA, 10.1007/s00592-022-01930-y, 59, 10, 1275-1286, 2022.10, Abstract

Aims: Pancreatic β-cell apoptosis may be involved in the onset and progression of type 2 diabetes mellitus, although its mechanism remains unclear. We previously demonstrated that macrophage-derived interferon (IFN) β induced X-linked inhibitor of apoptosis-associated factor 1 (XAF1) expression in β-cells and accelerated β-cell apoptosis in vitro. Here, we explored the effects of XAF1 on β-cell function and progression of diabetes in vivo.

Methods: Pancreatic β-cell-selective XAF1 overexpressing (Xaf1 Tg) mice were generated. Xaf1 Tg mice and their wild-type (WT) littermates were fed either a normal diet or a 40% or 60% high-fat diet (HFD). The effects of β-cell XAF1 on β-cell apoptosis and exacerbation of diabetes were investigated.

Results: Palmitic acid induced IFNβ expression in macrophages, and HFD intake promoted macrophage infiltration in pancreatic islets, both of which cooperatively upregulated XAF1 expression in mouse islets. Furthermore, HFD-fed Xaf1 Tg mice demonstrated increased β-cell apoptosis, lowered insulin expression, and impaired glucose tolerance compared with WT mice fed the same diet. These effects were more pronounced in the 60%HFD group than in the 40%HFD group.

Conclusions: Pancreatic β-cell XAF1 expression was enhanced via HFD-induced, macrophage-derived IFNβ, which promoted β-cell apoptosis and led to a reduction in insulin secretion and progression of diabetes. To our knowledge, this is the first report to demonstrate an association between pancreatic β-cell XAF1 overexpression and exacerbation of diabetes, thus providing insight into the mechanism of β-cell mass reduction in diabetes.

Keywords: High-fat diet; Interferon β; X-linked inhibitor of apoptosis–associated factor 1; β-cell apoptosis..


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