中村 恭子(ナカムラ キョウコ)

薬学総合研究所講師

Last Updated :2024/07/20

■教員コメント

コメント

糖尿病発症および細胞増殖に関わる研究を行っている。

■研究者基本情報

学位

  • 生命科学博士

研究キーワード

  • 肝糖代謝   ストレス   IGFBP-1   肝臓代謝   糖尿病   血管内皮前駆細胞   血管新生   SHRSP   

現在の研究分野(キーワード)

糖尿病発症および細胞増殖に関わる研究を行っている。

研究分野

  • ライフサイエンス / 栄養学、健康科学
  • ライフサイエンス / 代謝、内分泌学

■経歴

経歴

  • 2013年  近畿大学医学部助教

■研究活動情報

論文

  • Kyoko Nakamura
    Drug Discoveries & Therapeutics 16 4 191 - 195 2022年09月 [査読有り]
  • Yuko Okamatsu-Ogura; Keigo Fukano; Ayumi Tsubota; Junko Nio-Kobayashi; Kyoko Nakamura; Masami Morimatsu; Hiroshi Sakaue; Masayuki Saito; Kazuhiro Kimura
    SCIENTIFIC REPORTS 7 1 2017年07月 [査読有り]
     
    We previously reported brown adipocytes can proliferate even after differentiation. To test the involvement of mature adipocyte proliferation in cell number control in fat tissue, we generated transgenic (Tg) mice over-expressing cell-cycle inhibitory protein p27 specifically in adipocytes, using the aP2 promoter. While there was no apparent difference in white adipose tissue (WAT) between wild-type (WT) and Tg mice, the amount of brown adipose tissue (BAT) was much smaller in Tg mice. Although BAT showed a normal cellular morphology, Tg mice had lower content of uncoupling protein 1 (UCP1) as a whole, and attenuated cold exposure-or beta 3-adrenergic receptor (AR) agonist-induced thermogenesis, with a decrease in the number of mature brown adipocytes expressing proliferation markers. An agonist for the beta 3-AR failed to increase the number of proliferating brown adipocytes, UCP1 content in BAT, and oxygen consumption in Tg mice, although the induction and the function of beige adipocytes in inguinal WAT from Tg mice were similar to WT mice. These results show that brown adipocyte proliferation significantly contributes to BAT development and adaptive thermogenesis in mice, but not to induction of beige adipocytes.
  • Kyoko Nakamura; Osamu Muraoka
    BioScience Trends 11 6 688 - 693 2017年 [査読有り]
     
    We developed electrolyzed water (EW) using carbon electrodes and investigated the ability of the developed EW to inhibit the proliferation of human cervical carcinoma HeLa cells. We observed that EW-containing media inhibited HeLa cell proliferation. Many very small black dots were produced in EW and these were associated with the inhibitory effect on the cell proliferation. Furthermore, the very small black dots that could inhibit cell proliferation were produced only at pH 3 to 3.5 of EW. Additional experiments showed that this inhibition of proliferation is reversible. These results suggest that the effect of EW on HeLa cells is cytostatic and not cytotoxic. Thus, our results indicate that the EW developed in this study may be used to inhibit cell proliretation.
  • 中村 恭子; 赤木 淳二; 石伏 史明; 谷 恭輔; 森川 敏生; Pongpriyadacha Yutana; 村岡 修; 早川 堯夫; 角谷 晃司
    生薬学雑誌 69 2 53 - 58 2015年 [査読有り]
  • 大和シャクヤクの休眠打破と人工栽培に関する研究
    中村 恭子; 大野 加奈; 瀧川 義浩; 角谷 晃司
    薬用植物研究 37 1 22 - 28 2015年 [査読有り]
  • Chintan K. Kikani; Erik V. Verona; Jiyoon Ryu; Yanying Shen; Qingqing Ye; Li Zheng; Ziliang Qian; Hiroshi Sakaue; Kyoko Nakamura; Jie Du; Qunsheng Ji; Wataru Ogawa; Lu-Zhe Sun; Lily Q. Dong; Feng Liu
    SCIENCE SIGNALING 5 249 2012年11月 [査読有り]
     
    Enhanced activation of phosphoinositide 3-kinase (PI3K) is a hallmark of many human tumors because it promotes cell proliferation and survival through several mechanisms. One of these mechanisms is the phosphorylation of the serine and threonine kinase Akt at the cytosolic side of the plasma membrane by phosphoinositide-dependent protein kinase 1 (PDK1), which is recruited and activated by binding to the phosphoinositides produced by PI3K. We previously demonstrated increased nuclear accumulation of PDK1 in cells with enhanced PI3K activity. We report that nuclear PDK1 promoted cell proliferation by suppressing FOXO3A-dependent transcription of the gene encoding p27(Kip1) (an inhibitor of cell cycle progression), whereas it enhanced cell survival by inhibiting the activation of c-Jun amino-terminal kinase. Cells with nuclear-localized PDK1 showed anchorage-independent growth, and when injected into mice, these cells induced the formation of solid tumors. In human prostate tumors, cytoplasmic localization of PDK1 correlated only with early-stage, low-risk tumors, whereas nuclear PDK1 localization correlated with high-risk tumors. Together, our findings suggest a role for nuclear-translocated PDK1 in oncogenic cellular transformation and tumor progression in mice and humans.
  • Mei-Fang Zhong; Wei-Li Shen; Masaki Tabuchi; Kyoko Nakamura; Yi-Chen Chen; Cong-Zhen Qiao; Jin He; Jie Yang; Chuan Zhang; Zdravko Kamenov; Hideaki Higashino; Hong Chen
    EXPERIMENTAL DIABETES RESEARCH 2012年 [査読有り]
     
    We investigated large vessel function in lean Goto-Kakizaki diabetic rats (GK) and Otsuka Long-Evans Tokushima Fatty diabetic rats (OLETF) with possible roles of hyperglycemia/hyperosmolarity and insulin. Both young and old GK showed marked hyperglycemia with normal insulin level and well-preserved endothelium-dependent and endothelium-independent vasodilation in aorta and carotid artery. There were significant elevations in endothelial/inducible nitric oxide synthase (eNOS/iNOS) and inducible/constitutive heme oxygenase (HO-1/HO-2) in GK. The endothelium-dependent vasodilation in GK was inhibited partly by NOS blockade and completely by simultaneous blocking of HO and NOS. In contrast, OLETF showed hyperinsulinemia and mild hyperglycemia but significant endothelium dysfunction beginning at early ages with concomitantly reduced eNOS. Insulin injection corrected hyperglycemia in GK but induced endothelium dysfunction and intima hyperplasia. Hyperglycemia/hyperosmolarity in vitro enhanced vessel eNOS/HO. We suggest that hyperinsulinemia plays a role in endothelium dysfunction in obese diabetic OLETF, while hyperglycemia/hyperosmolarity-induced eNOS/HO upregulation participates in the adaptation of endothelium function in lean diabetic GK.
  • Mei-Fang Zhong; Wei-Li Shen; Masaki Tabuchi; Kyoko Nakamura; Yi-Chen Chen; Cong-Zhen Qiao; Jin He; Jie Yang; Chuan Zhang; Zdravko Kamenov; Hideaki Higashino; Hong Chen
    EXPERIMENTAL DIABETES RESEARCH 2012 42902  2012年 [査読有り]
     
    We investigated large vessel function in lean Goto-Kakizaki diabetic rats (GK) and Otsuka Long-Evans Tokushima Fatty diabetic rats (OLETF) with possible roles of hyperglycemia/hyperosmolarity and insulin. Both young and old GK showed marked hyperglycemia with normal insulin level and well-preserved endothelium-dependent and endothelium-independent vasodilation in aorta and carotid artery. There were significant elevations in endothelial/inducible nitric oxide synthase (eNOS/iNOS) and inducible/constitutive heme oxygenase (HO-1/HO-2) in GK. The endothelium-dependent vasodilation in GK was inhibited partly by NOS blockade and completely by simultaneous blocking of HO and NOS. In contrast, OLETF showed hyperinsulinemia and mild hyperglycemia but significant endothelium dysfunction beginning at early ages with concomitantly reduced eNOS. Insulin injection corrected hyperglycemia in GK but induced endothelium dysfunction and intima hyperplasia. Hyperglycemia/hyperosmolarity in vitro enhanced vessel eNOS/HO. We suggest that hyperinsulinemia plays a role in endothelium dysfunction in obese diabetic OLETF, while hyperglycemia/hyperosmolarity-induced eNOS/HO upregulation participates in the adaptation of endothelium function in lean diabetic GK.
  • Tomoki Nagare; Hiroshi Sakaue; Michihiro Matsumoto; Yongheng Cao; Kenjiro Inagaki; Mashito Sakai; Yasuhiro Takashima; Kyoko Nakamura; Toshiyuki Mori; Yuko Okada; Yasushi Matsuki; Eijiro Watanabe; Kazutaka Ikeda; Ryo Taguchi; Naomi Kamimura; Shigeo Ohta; Ryuji Hiramatsu; Masato Kasuga
    JOURNAL OF BIOLOGICAL CHEMISTRY 286 43 37458 - 37469 2011年10月 [査読有り]
     
    Kruppel-like factor 15 (KLF15), a member of the Kruppel-like factor family of transcription factors, has been found to play diverse roles in adipocytes in vitro. However, little is known of the function of KLF15 in adipocytes in vivo. We have now found that the expression of KLF15 in adipose tissue is down-regulated in obese mice, and we therefore generated adipose tissue-specific KLF15 transgenic (aP2-KLF15Tg) mice to investigate the possible contribution of KLF15 to various pathological conditions associated with obesity in vivo. The aP2-KLF15 Tg mice manifest insulin resistance and are resistant to the development of obesity induced by maintenance on a high fat diet. However, they also exhibit improved glucose tolerance as a result of enhanced insulin secretion. Furthermore, this enhancement of insulin secretion was shown to result from down-regulation of the expression of stearoyl-CoA desaturase 1 (SCD1) in white adipose tissue and a consequent reduced level of oxidative stress. This is supported by the findings that restoration of SCD1 expression in white adipose tissue of aP2-KLF15 Tg mice exhibited increased oxidative stress in white adipose tissue and reduced insulin secretion with hyperglycemia. Our data thus provide an example of cross-talk between white adipose tissue and pancreatic beta cells mediated through modulation of oxidative stress.
  • Changes of endothelium-dependent vasodilation in aortae from obese and non-obese type 2 diabetic rats and the roles of hyperglycemia/hyperosmolarity.
    Chen YC; 田渕 正樹; 中村 恭子; 東野 英明; Zhou D Zhong MF; Yang J Teng; L; Gu JZ; Chen H
    Chin. J. Hypertens. 19 6 529 - 537 2011年06月 [査読有り]
  • T. Kurita; K. Nakamura; M. Tabuchi; M. Orita; K. Ooshima; H. Higashino
    Journal of Medical Sciences 11 1 30 - 38 2011年 [査読有り]
     
    The details of pharmacological mechanisms of Gorei-san, a traditional Japanese Kampo medicine, remains to be clarified, although it has been used for diuretic and hydrostatic purposes. From these circumstances, the effects of this medicine on the expressions of aquaporin (AQP) 1, 2, 3, 4 and vasopressin 2 receptor (V2R) mRNAs were investigated in relation to diuresis and water balance regulation in the kidney and brain. Gorei-san extract decocted with hot water was given to rats loaded with 50 mL kg-1 volume of physiological saline and AQP1, 2, 3, 4 and V2R mRNAs were measured with real-time polymerase chain reaction (PCR) in the cortex and the medulla of kidney and the forebrain. A low dose of Gorei-san extract (100 mg kg-1) led to an increase in urine excretion and lower AQP3 mRNA expression in the cortex as well as lower expression of AQP2 and AQP3 mRNAs in the medulla of kidney, whereas no change in V2R mRNA expression was observed. AQP1 mRNA expression decreased in the forebrain of rats loaded with an excess volume of physiological saline compared with rats not loaded with excess saline and given no agent. A low dose of Gorei-san extract increased urine excretion volume, probably due to the downregulation of AQP3 mRNA in the cortex and downregulation of AQP2 and AQP3 mRNAs in the medulla of the kidney, in which changes were not related to V2R mRNA expression. An excess volume of physiological saline given to rats caused an inhibition of AQP1 mRNA expression in the forebrain, which probably functioned to maintain the water balance in a hyper-hydrous state.
  • Kyoko Nakamura; Hiroshi Sakaue; Akihiko Nishizawa; Yasushi Matsuki; Hideyuki Gomi; Eijiro Watanabe; Ryuji Hiramatsu; Mimi Tamamori-Adachi; Shigetaka Kitajima; Tetsuo Noda; Wataru Ogawa; Masato Kasuga
    JOURNAL OF BIOLOGICAL CHEMISTRY 283 25 17702 - 17711 2008年06月 [査読有り]
     
    PDK1 (3-phosphoinositide-dependent protein kinase 1) is a key mediator of signaling by phosphoinositide 3-kinase. To gain insight into the physiological importance of PDK1 in cell proliferation and cell cycle control, we established immortalized mouse embryonic fibroblasts (MEFs) from mice homozygous for a "floxed" allele of Pdk1 and from wild-type mice. Introduction of Cre recombinase by retrovirus-mediated gene transfer resulted in the depletion of PDK1 in Pdk1(lox/lox) MEFs but not in Pdk1(+/+) MEFs. The insulin-like growth factor-1-induced phosphorylation of various downstream effectors of PDK1, including Akt, glycogen synthase kinase 3, ribosomal protein S6, and p70 S6 kinase, was markedly inhibited in the PDK1-depleted (Pdk1-KO) MEFs. The rate of serum-induced cell proliferation was reduced; progression of the cell cycle from the G(0)-G(1) phase to the S phase was delayed, and cell cycle progression at G(2)-M phase was impaired in Pdk1-KO MEFs. These cells also manifested an increased level of p27(Kip1) expression and a reduced level of cyclin D1 expression during cell cycle progression. The defect in cell cycle progression from the G(0)-G(1) to the S phase in Pdk1-KO MEFs was rescued by forced expression of cyclin D1, whereas rescue of the defect in G(2)-M progression in these cells required both overexpression of cyclin D1 and depletion of p27(Kip1) by RNA interference. These data indicate that PDK1 plays an important role in cell proliferation and cell cycle progression by controlling the expression of both cyclin D1 and p27(Kip1).
  • Takahiro Seki; Naoki Irie; Kyoko Nakamura; Hiroshi Sakaue; Wataru Ogawa; Masato Kasuga; Hideyuki Yamamoto; Shiho Ohmori; Naoaki Saito; Norio Sakai
    GENES TO CELLS 11 9 1051 - 1070 2006年09月 [査読有り]
     
    To elucidate the role of 3-phosphoinositide-dependent protein kinase-1 (PDK1) in cellular signaling, we constructed and expressed a pseudosubstrate of PDK1, designated as delta AL-PIF, and characterized its properties in cultured cells. delta AL-PIF consists of two fused proteins of the protein kinase C delta (delta PKC) activation loop (delta AL) and PDK1-interacting fragment (PIF). The phosphorylation of delta AL-PIF was detected with anti-delta PKC phospho-Thr(505)-specific antibody and was increased in proportion to the expression level of co-expressed GST-PDK1, indicating that it acts as a pseudosubstrate of PDK1. In cells expressing delta AL-PIF, basal phosphorylation level at the activation loop of PKB alpha, delta PKC and gamma PKC was reduced, compared with that in control cells, suggesting that delta AL-PIF functions as an inhibitory molecule for PDK1. delta AL-PIF affected the stability, translocation and endogenous activity of PKCs. These effects of delta AL-PIF on gamma PKC properties were confirmed by investigation using conditioned PDK1 knockout cells. Furthermore, apoptosis frequently occurred in cells expressing delta AL-PIF for 3 days. These findings revealed that delta AL-PIF served as an effective pseudosubstrate and an inhibitory molecule for PDK1, suggesting that this molecule can be used as a tool for investigating PDK-mediated cellular functions as well as being applicable for anti-cancer therapy.
  • γPKCのトランスロケーションと発現量の調節に関するPDK1の役割 PDK1ノックアウト細胞を用いた検討
    関 貴弘; 天野 託; 松林 弘明; 中村 恭子; 阪上 浩; 小川 渉; 春日 雅人; 大森 志保; 斎藤 尚亮; 酒井 規雄
    日本薬理学雑誌 127 1 25P - 25P (公社)日本薬理学会 2006年01月 [査読有り]
  • Toshiyuki Mori; Hiroshi Sakaue; Hiroshi Sakaue; Haruhisa Iguchi; Hideyuki Gomi; Yuko Okada; Yasuhiro Takashima; Kyoko Nakamura; Takehiro Nakamura; Toshimasa Yamauchi; Naoto Kubota; Takashi Kadowaki; Yasushi Matsuki; Wataru Ogawa; Ryuji Hiramatsu; Masato Kasuga
    Journal of Biological Chemistry 280 13 12867 - 12875 2005年04月 [査読有り]
     
    Krüppel-like zinc finger transcription factors (KLFs) play diverse roles during cell differentiation and development in mammals. We have now shown by microarray analysis that expression of the KLF15 gene is markedly up-regulated during the differentiation of 3T3-L1 preadipocytes into adipocytes. Inhibition of the function of KLF15, either by expression of a dominant negative mutant or by RNA interference, both reduced the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and blocked adipogenesis in 3T3-L1 preadipocytes exposed to inducers of adipocyte differentiation. However, the dominant negative mutant of KLF15 did not affect the expression of CCAAT/enhancer-binding protein beta (C/EBPbeta) elicited by inducers of differentiation in 3T3-L1 preadipocytes. In addition, ectopic expression of KLF15 in NIH 3T3 or C2C12 cells triggered both lipid accumulation and the expression of PPARgamma in the presence of inducers of adipocyte differentiation. Ectopic expression of C/EBPbeta, C/EBPdelta, or C/EBPalpha in NIH 3T3 cells also elicited the expression of KLF15 in the presence of inducers of adipocyte differentiation. Moreover, KLF15 and C/EBPalpha acted synergistically to increase the activity of the PPARgamma2 gene promoter in 3T3-L1 adipocytes. Our observations thus demonstrate that KLF15 plays an essential role in adipogenesis in 3T3-L1 cells through its regulation of PPAR gamma expression.
  • Kyoko Nakamura; Takao Senda; Kenzo Sato; Shigeo Mori; Masatsugu Moriyama
    Pathobiology 72 4 191 - 202 2005年 [査読有り]
     
    <i>Objectives:</i> The dysregulated overexpression of BCL10 that results from a specific chromosomal translocation t(1;14)(p22;q32) in mucosa-associated lymphoid tissue lymphoma has been shown to activate nuclear factor (NF)-ĸB, which may promote growth and survival in tumor cells. Accordingly, the molecular mechanisms underlying NF-ĸB activation may be responsible for lymphomagenesis. The aim of this study was to determine the molecular mechanisms underlying NF-ĸB activation by BCL10 overexpression. <i>Methods:</i> HeLa or COS-1 cells were transfected with BCL10, intracellular localization of BCL10 and the activation of NF-ĸB were analyzed. <i>Results:</i> BCL10 expressed at a high level exhibited a filamentous distribution at the perinuclear region, whereas BCL10 at a low level of expression displayed a diffuse cytoplasmic distribution. Furthermore, the BCL10-mediated NF-ĸB activation was efficiently inhibited by a Ca<sup>2+</sup> chelating agent or a Ca<sup>2+</sup> channel blocker. We also found that amino acids (107–119) of BCL10 are required for the formation of filamentous structures at the perinuclear region and NF-ĸB activation. <i>Conclusion:</i> These findings suggest that the filamentous pattern of overexpressed BCL10 at the perinuclear region adjacent to the endoplasmic reticulum is important for the BCL10-mediated NF-ĸB activation.
  • Role of MAPK phosphatase-1 (MKP-1) in adipocyte differentiation
    Hiroshi Sakaue; Wataru Ogawa; Wataru Ogawa; Takehiro Nakamura; Toshiyuki Mori; Kyoko Nakamura; Masato Kasuga
    Journal of Biological Chemistry 279 39951 - 39957 2004年09月 [査読有り]
  • Kyoko Nakamura; Chisato Nakada; Kengo Takeuchi; Mitsuhiko Osaki; Kohei Shomori; Shinsuke Kato; Eisaku Ohama; Kenzo Sato; Masashi Fukayama; Shigeo Mori; Hisao Ito; Masatsugu Moriyama
    Pathobiology 70 4 197 - 203 2002年 [査読有り]
     
    <i>Objectives:</i> Cardiac ankyrin repeat protein, CARP, is a protein that is restrictedly expressed in the heart but barely expressed in skeletal muscles. Since CARP is induced by pressure overload to the heart, it is proposed to be a genetic marker for cardiac hypertrophy. We recently identified a novel protein, ankyrin repeat protein with PEST and proline-rich region (ARPP), which is homologous to CARP and is preferentially expressed in type 1 skeletal muscle fibers (cf. slow fibers). We also found that both ARPP and CARP expression is induced in experimentally denervated skeletal muscles in mice. Based on these findings, we hypothesized that their expression may be induced in skeletal muscles in neurodegenerating disease. This work aimed to determine the expression pattern of ARPP and CARP in amyotrophic lateral sclerosis (ALS). <i>Methods:</i> In this study, we immunohistochemically analyzed the expression of ARPP and CARP in skeletal muscles of 9 ALS cases. <i>Results:</i> We found that CARP was aberrantly expressed in atrophic skeletal muscle fibers in ALS. Although ARPP-positive fibers were randomly scattered in a checkerboard-like pattern in normal skeletal muscle, this pattern was absent in ALS muscles. Furthermore, we also found that ARPP was expressed in fast myosin heavy chain-positive fibers (cf. type 2 fiber). <i>Conclusion:</i> These findings suggest that type-specific expression patterns of ARPP and CARP are altered in skeletal muscles of ALS.

MISC

  • 肝臓のGLP-1 受容体を介した食後高血糖の分子機序の解明
    中村 恭子 Medical Science Digest 46 (1) 50 -52 2020年01月 [査読有り][招待有り]
  • ResveratrolおよびFisetinによる誘導する抗加齢関連遺伝子の発現解析
    角谷 晃司; 西川 恵未; 中村 恵実; 中村 恭子; 瀧川 義浩; 早川 堯夫 日本生薬学会年会講演要旨集 61回 281 -281 2014年08月
  • Kyoko Nakamura; Masaki Tabuchi; Kana Ooshima; Atsuko Niwa; Hideo Takahashi JOURNAL OF PHARMACOLOGICAL SCIENCES 118 128P -128P 2012年
  • Masaki Tabuchi; Kana Ooshima; Hiroshi Sakaue; Kyoko Nakamura; Atsuko Niwa; Hideo Takahashi JOURNAL OF PHARMACOLOGICAL SCIENCES 118 85P -85P 2012年
  • 肥満・糖尿病発症における転写因子KLF15の役割
    永礼 智基; 阪上 浩; 岡田 裕子; 岡田 潮; 高島 康弘; 中村 恭子; 松木 泰; 平松 隆司; 渡辺 英二郎; 小川 渉; 春日 雅人 糖尿病 51 (Suppl.1) S -309 2008年04月
  • 脂肪細胞増殖機構を標的とした肥満・インスリン抵抗性治療の探索
    阪上 浩; 中村 武寛; 酒井 太門; 岡田 潮; 岡田 裕子; 高島 康弘; 永礼 智基; 中村 恭子; 春日 雅人; 吉田 智一; 川崎 由子; 石原 英樹 肥満研究 13 (Suppl.) 199 -199 2007年09月
  • p27KOマウスにおける高アディポネクチン血症と慢性炎症との関係
    岡田 潮; 阪上 浩; 中村 武寛; 酒井 太門; 岡田 裕子; 高島 康弘; 永禮 智基; 中村 恭子; 春日 雅人; 中山 啓一 肥満研究 13 (Suppl.) 308 -308 2007年09月
  • PI3Kおよび関連シグナル伝達分子の機能 グルコース代謝におけるPDK1の役割(Role of PDK1 in Glucose Metabolism)
    小川 渉; 井上 啓; 岡本 安生; 阪上 浩; 中村 恭子; 古川 健亮; 木戸 良明; 春日 雅人 日本発生生物学会・日本細胞生物学会合同大会要旨集 40回・59回 15 -15 2007年05月
  • インスリン抵抗性発症における小型脂肪細胞の意義
    阪上 浩; 中村 武寛; 酒井 太門; 岡田 潮; 岡田 裕子; 高島 康弘; 永禮 智基; 中村 恭子; 中山 敬一; 春日 雅人 糖尿病 50 (Suppl.1) S -219 2007年04月
  • 脂肪細胞増殖機構を標的とした肥満・インスリン抵抗性治療の探索
    中村 武寛; 阪上 浩; 酒井 太門; 岡田 潮; 岡田 裕子; 高島 康弘; 永礼 智基; 中村 恭子; 吉田 智一; 川崎 由子; 石原 英幹; 春日 雅人 糖尿病 50 (Suppl.1) S -222 2007年04月
  • 肥満・糖尿病発症におけるユビキチンリガーゼSkp2の役割
    阪上 浩; 酒井 太門; 中村 武寛; 岡田 潮; 岡田 裕子; 高島 康弘; 永礼 智基; 中村 恭子; 中山 啓子; 春日 雅人 日本臨床分子医学会学術総会プログラム・抄録集 43回 76 -76 2006年07月
  • 肥満・糖尿病発症におけるユビキチンリガーゼSkp2の役割
    酒井 太門; 阪上 浩; 中村 武寛; 岡田 潮; 岡田 裕子; 高島 康弘; 永礼 智基; 中村 恭子; 春日 雅人; 中山 啓子 糖尿病 49 (Suppl.1) S267 -S267 2006年04月
  • 肥満発症における脂肪細胞増殖時期の同定
    中村 武寛; 阪上 浩; 酒井 太門; 岡田 潮; 岡田 裕子; 高島 康弘; 永礼 智基; 中村 恭子; 春日 雅人 肥満研究 11 (Suppl.) 132 -132 2005年09月
  • 細胞成長(cell growth)制御におけるPDK-1の役割
    中村 恭子; 阪上 浩; 小川 渉; 春日 雅人 糖尿病 48 (Suppl.2) S137 -S137 2005年04月
  • 脂肪細胞の数とサイズを決定する細胞周期制御機構の糖代謝における重要性
    中村 武寛; 阪上 浩; 酒井 太門; 岡田 潮; 岡田 裕子; 高島 康弘; 森 要之; 中村 恭子; 小川 渉; 中山 敬一; 中山 啓子; 春日 雅人 Diabetes Frontier 15 (4) 574 -575 2004年08月
  • 脂肪細胞の数とサイズを決定する細胞周期制御機構の糖代謝における重要性
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  • 脂肪蓄積に関わる遺伝子解析の新展開 優位抑制型変異体及びsiRNAを用いた3T3-L1脂肪細胞分化機構における転写因子KLF15の機能解析
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共同研究・競争的資金等の研究課題

  • 日本学術振興会:科学研究費助成事業
    研究期間 : 2022年04月 -2025年03月 
    代表者 : 中村 恭子
  • 日本学術振興会:科学研究費助成事業
    研究期間 : 2018年04月 -2023年03月 
    代表者 : 中村 恭子
     
    申請者は、2 型糖尿病の発症に重要な要素の一つである食後高血糖に着目して研究を行っている。特に、食直後の急激な血糖値上昇に肝臓におけるグルカゴン様ペプチド-1 (GLP-1) シグナル系が関与している可能性を見出している。 本研究の目的は、2 型糖尿病モデルマウスを用いて、2 型糖尿病発症の前段階から発症過程において、固形状および粉状といった食餌の形状の違いがもたらす影響について明らかにしていくことである。自然発症 2 型糖尿病モデルマウスである ob/ob マウスを発症前段階の 4 週齢から発症段階の 8 週齢において食餌の形状による血糖値上昇に与える影響を検討するにあたり、医学部での動物実験を予定していたが、新型コロナウィルス感染症の流行拡大により、行うことが困難となったため、細胞レベルでの検討を行うための実験設備を整備した。
  • 日本学術振興会:科学研究費助成事業
    研究期間 : 2013年04月 -2017年03月 
    代表者 : 中村 恭子
     
    食後高血糖は食後の血糖値が一過性にに急上昇し、空腹時血糖値が正常または境界領域でも生じる。よって通常の健康診断では見逃される可能性があり、日本で糖尿病患者が増加の原因の一つではないかと考え食後高血糖の発症メカニズムを検討した。その結果、2型糖尿病モデルマウスであるob/obマウスでは、食後1時間の肝臓におけるcaveolin-1発現が低下し、GLP-1受容体発現が高まり、糖代謝に関与するGLP-1受容体の機能異常が考えられた。
  • 日本学術振興会:科学研究費助成事業
    研究期間 : 2012年04月 -2015年03月 
    代表者 : 高橋 英夫; 丹羽 淳子; 西堀 正洋; 劉 克約; 中村 恭子; 大島 佳奈
     
    High mobility group box1(HMGB1)は、免疫応答に大きく関与している。申請者らは、HMGB1が脳梗塞、アテローム性動脈硬化症などの原因因子で、抗HMGB1抗体でこれらを抑制できることを報告した。HMGB1の高血圧症の病態生理への関与はまだ明らかではないので、脳卒中易発症高血圧症自然発症ラット (SHRSP)を用いて検討してきた。血管内皮細胞障害が高血圧症の原因であるが,HMGB1の血管内皮細胞障害は確認出来なかったが、好中球活性化が血管内皮細胞障害を誘導する機序を解明することが出来た。好中球活性化制御因子を特定したので、高血圧症新規治療薬の開発に向けた研究を継続する。
  • 日本学術振興会:科学研究費助成事業
    研究期間 : 2009年 -2010年 
    代表者 : 中村 恭子
     
    本研究では、絶食・再摂食時における肝臓でのホルモンおよびストレス関連因子の遺伝子発現について解析した。その結果、2型糖尿病モデルマウスの肝臓では(1)インスリン様成長因子(IGF-1)発現の低下(2)IGF結合タンパク質-1(IGFBP-1)発現の増強(3)11β-ヒドロキシステロイドデヒドロゲナーゼ(11β-HSD1)の発現亢進(4)ERストレス関連因子の発現低下(5)glucagon-like peptide-1(GLP-1)の受容体発現の亢進が見出された。
  • 日本学術振興会:科学研究費助成事業
    研究期間 : 2008年 -2010年 
    代表者 : 丹羽 淳子; 東野 英明; 中村 恭子; 阪上 浩; 大島 佳奈
     
    運動療法の予防・治療効果の一因として造血幹細胞や血管内皮前駆細胞(EPC)、神経幹細胞の増加を予想し、ヒト本態性高血圧症病態モデルSHRSPを用いて検討した。運動群では発症前および発症後速やかに骨髄・末梢血中のEPCや造血幹細胞が増加し、脳病変部周囲の微小血管や神経幹細胞数も増加した。またEPCの誘導、移動に必須のCXCL12やVEGF、神経新生に関与するBDNFとそのシグナル分子ERKやCREBの活性化が認められた。

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