Faculty Profiles - ARIMA, Hiroshi

Papers - ARIMA, Hiroshi

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実臨床データに基づいた機械学習による低ナトリウム血症治療における血清ナトリウム濃度予測

木下珠希, 大山慎太郎, 萩原大輔, 有馬寛

医療情報学連合大会論文集 Vol. 42回 page： 1195 - 1200 2022.11

Differentiation of human induced pluripotent stem cells into hypothalamic vasopressin neurons with minimal exogenous signals and partial conversion to the naive state. Reviewed International journal

Hajime Ozaki, Hidetaka Suga, Mayu Sakakibara, Mika Soen, Natsuki Miyake, Tsutomu Miwata, Shiori Taga, Takashi Nagai, Mayuko Kano, Kazuki Mitsumoto, Takashi Miyata, Tomoko Kobayashi, Mariko Sugiyama, Takeshi Onoue, Hiroshi Takagi, Daisuke Hagiwara, Shintaro Iwama, Ryoichi Banno, Genzo Iguchi, Yutaka Takahashi, Keiko Muguruma, Haruhisa Inoue, Hiroshi Arima

Scientific reports Vol. 12 ( 1 ) page： 17381 - 17381 2022.10

Authorship：Last author Language：English Publishing type：Research paper (scientific journal)

Familial neurohypophyseal diabetes insipidus (FNDI) is a degenerative disease of vasopressin (AVP) neurons. Studies in mouse in vivo models indicate that accumulation of mutant AVP prehormone is associated with FNDI pathology. However, studying human FNDI pathology in vivo is technically challenging. Therefore, an in vitro human model needs to be developed. When exogenous signals are minimized in the early phase of differentiation in vitro, mouse embryonic stem cells (ESCs)/induced pluripotent stem cells (iPSCs) differentiate into AVP neurons, whereas human ESCs/iPSCs die. Human ESCs/iPSCs are generally more similar to mouse epiblast stem cells (mEpiSCs) compared to mouse ESCs. In this study, we converted human FNDI-specific iPSCs by the naive conversion kit. Although the conversion was partial, we found improved cell survival under minimal exogenous signals and differentiation into rostral hypothalamic organoids. Overall, this method provides a simple and straightforward differentiation direction, which may improve the efficiency of hypothalamic differentiation.

DOI： 10.1038/s41598-022-22405-8

Web of Science

PubMed

機械学習を用いた重症低ナトリウム血症の治療予測システムの構築

木下珠希, 萩原大輔, 大山慎太郎, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 2 ) page： 554 - 554 2022.10

Changing the Name of Diabetes Insipidus: A Position Statement of the Working Group to Consider Renaming Diabetes Insipidus

Arima, H; Cheetham, T; Christ-Crain, M; Cooper, DL; Drummond, JB; Gurnell, M; Levy, M; McCormack, A; Newell-Price, JD; Verbalis, JG; Wass, J

HORMONE RESEARCH IN PAEDIATRICS Vol. 96 ( 4 ) page： 423 - 425 2022.9

Elevated TSH level, TgAb and prior use of ramucirumab or TKIs as risk factors for thyroid dysfunction in PD-L1 blockade. Reviewed International journal

Tomoko Kobayashi, Shintaro Iwama, Ayana Yamagami, Yoshinori Yasuda, Takayuki Okuji, Masaaki Ito, Xin Zhou, Masahiko Ando, Takeshi Onoue, Takashi Miyata, Mariko Sugiyama, Daisuke Hagiwara, Hidetaka Suga, Ryoichi Banno, Tetsunari Hase, Masahiro Morise, Takanori Ito, Toyone Kikumori, Megumi Inoue, Yuichi Ando, Norikazu Masuda, Hiroki Kawashima, Naozumi Hashimoto, Hiroshi Arima

The Journal of clinical endocrinology and metabolism Vol. 107 ( 10 ) page： E4115 - E4123 2022.9

Authorship：Last author Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Thyroid dysfunction is frequently caused by treatment with anti-programmed cell death-1 ligand 1 antibodies (PD-L1-Abs) as well as anti-cancer drugs, including ramucirumab (RAM) and multi-targeted tyrosine kinase inhibitors (multi-TKIs), which are often used prior to PD-L1-Ab treatment in cancer patients. METHODS: A total of 148 patients treated with PD-L1-Abs were evaluated for anti-thyroid antibodies at baseline and for thyroid function every six weeks for 24 weeks after treatment initiation and then were observed until the visits stopped. RESULTS: Of the 148 patients, 15 (10.1%) developed thyroid dysfunction after PD-L1-Ab treatment (destructive thyroiditis in eight and hypothyroidism without preceding thyrotoxicosis in seven). The prevalences of an elevated thyroid-stimulating hormone (TSH) level at baseline (3/15 [20.0%] vs. 4/133 [3.0%], p < 0.05), positive anti-thyroglobulin antibodies (TgAb) at baseline (4/15 [26.7%] vs. 5/133 [3.8%], p < 0.05) and prior treatment with RAM or multi-TKIs (3/15 [20.0%] vs. 5/133 [3.8%], p < 0.05) were significantly higher in patients with versus without thyroid dysfunction. In a multivariate analysis, elevated TSH level at baseline, TgAb positivity at baseline and prior treatment with RAM or multi-TKIs were significantly associated with the development of thyroid dysfunction, with odds ratios of 7.098 (95% confidence interval [CI], 1.154-43.638), 11.927 (95% CI, 2.526-56.316) and 8.476 (95% CI, 1.592-45.115), respectively. CONCLUSIONS: The results of this real-world study suggest that the risk of thyroid dysfunction induced by PD-L1-Abs can be predicted by the TSH level at baseline, TgAb positivity at baseline and prior treatment with RAM or multi-TKIs.

DOI： 10.1210/clinem/dgac467

Web of Science

PubMed

Inflammation in VTA Caused by HFD Induces Activation of Dopaminergic Neurons Accompanied by Binge-like Eating. Reviewed International journal

Runan Sun, Mariko Sugiyama, Sixian Wang, Mitsuhiro Kuno, Tomoyuki Sasaki, Tomonori Hirose, Takashi Miyata, Tomoko Kobayashi, Taku Tsunekawa, Takeshi Onoue, Yoshinori Yasuda, Hiroshi Takagi, Daisuke Hagiwara, Shintaro Iwama, Hidetaka Suga, Hiroshi Arima

Nutrients Vol. 14 ( 18 ) 2022.9

Authorship：Last author Language：English Publishing type：Research paper (scientific journal)

Binge eating is a characteristic symptom observed in obese individuals that is related to dysfunction of dopaminergic neurons (DNs). Intermittent administration of a high-fat diet (HFD) is reported to induce binge-like eating, but the underlying mechanisms remain unclear. We generated dopaminergic neuron specific IKKβ deficient mice (KO) to examine the effects of inflammation in DNs on binge-like eating under inflammatory conditions associated with HFD. After administration of HFD for 4 weeks, mice were fasted for 24 h, and then the consumption of HFD was measured for 2 h. We also evaluated that the mRNA expressions of inflammatory cytokines, glial markers, and dopamine signaling-related genes in the ventral tegmental area (VTA) and striatum. Moreover, insulin was administered intraventricularly to assess downstream signaling. The consumption of HFD was significantly reduced, and the phosphorylation of AKT in the VTA was significantly increased in female KO compared to wild-type (WT) mice. Analyses of mRNA expressions revealed that DNs activity and inflammation in the VTA were significantly decreased in female KO mice. Thus, our data suggest that HFD-induced inflammation with glial cell activation in the VTA affects DNs function and causes abnormal eating behaviors accompanied by insulin resistance in the VTA of female mice.

DOI： 10.3390/nu14183835

Web of Science

PubMed

Protein Tyrosine Phosphatase 1B Deficiency Improves Glucose Homeostasis in Insulin-Dependent Diabetes Mellitus Treated with Leptin. Reviewed International journal

Yoshihiro Ito, Runan Sun, Hiroshi Yagimuma, Keigo Taki, Akira Mizoguchi, Tomoko Kobayashi, Mariko Sugiyama, Takeshi Onoue, Taku Tsunekawa, Hiroshi Takagi, Daisuke Hagiwara, Shintaro Iwama, Hidetaka Suga, Hiroyuki Konishi, Hiroshi Kiyama, Hiroshi Arima, Ryoichi Banno

Diabetes Vol. 71 ( 9 ) page： 1902 - 1914 2022.9

Language：English Publishing type：Research paper (scientific journal)

Leptin, a hormone secreted by adipocytes, exhibits therapeutic potential for the treatment of insulin-dependent diabetes mellitus (IDDM). Protein tyrosine phosphatase 1B (PTP1B) is a key enzyme that negatively regulates leptin receptor signaling. Here, the role of PTP1B in the treatment of IDDM was investigated using PTP1B deficient (KO) mice and a PTP1B inhibitor. IDDM wild-type (WT) mice induced by streptozotocin showed marked hyperglycemia compared to non-IDDM WT mice. KO mice displayed significantly improved glucose metabolism equivalent to non-IDDM WT mice, whereas peripheral or central administration of leptin partially improved glucose metabolism in IDDM WT mice. Peripheral combination therapy of leptin and a PTP1B inhibitor in IDDM WT mice improved glucose metabolism to the same level as non-IDDM WT mice. Leptin was shown to act on the arcuate nucleus in the hypothalamus to suppress gluconeogenesis in liver and enhance glucose uptake in both brown adipose tissue and soleus muscle via the sympathetic nervous system. These effects were enhanced by PTP1B deficiency. Thus, treatment of IDDM with leptin, PTP1B deficiency or a PTP1B inhibitor was shown to enhance leptin activity in the hypothalamus to improve glucose metabolism. These findings suggest a potential alternative therapy for IDDM.

DOI： 10.2337/db21-0953

Web of Science

PubMed

Disease Modeling of Pituitary Adenoma Using Human Pluripotent Stem Cells Reviewed Open Access

Ryusaku Matsumoto, Hidetaka Suga, Hiroshi Arima, Takuya Yamamoto

Cancers Vol. 14 ( 15 ) page： 3660 2022.8

Language：English Publishing type：Research paper (scientific journal)

Pituitary adenomas are characterized by abnormal growth in the pituitary gland. Surgical excision is the first-line treatment for functional (hormone-producing) pituitary adenomas, except for prolactin-producing adenomas; however, complete excision is technically challenging, and many patients require long-term medication after the treatment. In addition, the pathophysiology of pituitary adenomas, such as tumorigenesis, has not been fully understood. Pituitary adenoma pathophysiology has mainly been studied using animal models and animal tumor-derived cell lines. Nevertheless, experimental studies on human pituitary adenomas are difficult because of the significant differences among species and the lack of reliable cell lines. Recently, several methods have been established to differentiate pituitary cells from human pluripotent stem cells (hPSCs). The induced pituitary hormone-producing cells retain the physiological properties already lost in tumor-derived cell lines. Moreover, CRISPR/Cas9 systems have expedited the introduction of causative gene mutations in various malignant tumors into hPSCs. Therefore, hPSC-derived pituitary cells have great potential as a novel platform for studying the pathophysiology of human-specific pituitary adenomas and developing novel drugs. This review presents an overview of the recent progresses in hPSC applications for pituitary research, functional pituitary adenoma pathogenesis, and genome-editing techniques for introducing causative mutations. We also discuss future applications of hPSCs for studying pituitary adenomas.

DOI： 10.3390/cancers14153660

EpCAM Is a Surface Marker for Enriching Anterior Pituitary Cells From Human Hypothalamic-Pituitary Organoids Reviewed

Kodani, Y; Kawata, M; Suga, H; Kasai, T; Ozone, C; Sakakibara, M; Kuwahara, A; Taga, S; Arima, H; Kameyama, T; Saito, K; Nakashima, A; Nagasaki, H

FRONTIERS IN ENDOCRINOLOGY Vol. 13 page： 941166 2022.7

The multifaceted role of ATF4 in regulating glucose-stimulated insulin secretion Reviewed

Sobajima, M; Miyake, M; Hamada, Y; Tsugawa, K; Oyadomari, M; Inoue, R; Shirakawa, J; Arima, H; Oyadomari, S

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Vol. 611 page： 165 - 171 2022.6

Immune checkpoint inhibitor-related thyroid dysfunction Invited Reviewed

Shintaro Iwama, Tomoko Kobayashi, Yoshinori Yasuda, Hiroshi Arima

Best Practice & Research Clinical Endocrinology & Metabolism Vol. 36 ( 3 ) page： 101660 - 101660 2022.5

イピリムマブ・ニボルマブ併用療法による甲状腺障害の臨床的特徴と高リスクマーカー

小林朋子, 岩間信太郎, 山上綾菜, 伊藤雅晃, 奥地剛之, 安田康紀, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 1 ) page： 306 - 306 2022.4

抗PD-1抗体療法開始前の抗甲状腺抗体の存在は非小細胞肺癌患者の生存期間延長と相関する

奥地剛之, 岩間信太郎, 山上綾菜, Zhou Xin, 伊藤雅晃, 小林朋子, 安田康紀, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 1 ) page： 305 - 305 2022.4

ストレプトゾトシン糖尿病マウスにおける抗PD-1抗体の大腸癌細胞株に対する抗腫瘍効果低下とケモカインの関連

伊藤雅晃, 岩間信太郎, 奥地剛之, 安田康紀, 山上綾菜, 周シン, 小林朋子, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 1 ) page： 289 - 289 2022.4

部分的なバソプレシン分泌不全状態ではミネラルコルチコイドの作用により多尿が顕在化する

栗本隼樹, 高木博史, 津村哲郎, 蓬臺優一, 川口頌平, 宮田崇, 萩原大輔, 須賀英隆, 安藤史顕, 内田信一, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 1 ) page： 278 - 278 2022.4

Increased Risk of Thyroid Dysfunction by PD-1 and CTLA-4 Blockade in Patients Without Thyroid Autoantibodies at Baseline. Reviewed International journal

Shintaro Iwama, Tomoko Kobayashi, Yoshinori Yasuda, Takayuki Okuji, Masaaki Ito, Masahiko Ando, Xin Zhou, Ayana Yamagami, Takeshi Onoue, Yohei Kawaguchi, Takashi Miyata, Mariko Sugiyama, Hiroshi Takagi, Daisuke Hagiwara, Hidetaka Suga, Ryoichi Banno, Tetsunari Hase, Masahiro Morise, Keiko Wakahara, Kenji Yokota, Masashi Kato, Naoki Nishio, Chie Tanaka, Kazushi Miyata, Atsushi Ogura, Takanori Ito, Tsunaki Sawada, Tomoya Shimokata, Kaoru Niimi, Fumiharu Ohka, Masatoshi Ishigami, Momokazu Gotoh, Naozumi Hashimoto, Ryuta Saito, Hitoshi Kiyoi, Hiroaki Kajiyama, Yuichi Ando, Hideharu Hibi, Michihiko Sone, Masashi Akiyama, Yasuhiro Kodera, Hiroshi Arima

The Journal of clinical endocrinology and metabolism Vol. 107 ( 4 ) page： E1620 - E1630 2022.3

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Previous studies showed that although the risk of thyroid dysfunction [thyroid immune-related adverse events (irAEs)] induced by anti-programmed cell death-1 antibodies (PD-1-Ab) was as low as 2% to 7% in patients negative for anti-thyroid antibodies (ATAs) at baseline, it was much higher (30%-50%) in patients positive for ATAs. However, whether a similar increase occurs with combination therapy using PD-1-Ab plus anti-cytotoxic T-lymphocyte antigen-4 antibody (CTLA-4-Ab) is unknown. METHODS: A total of 451 patients with malignancies treated with PD-1-Ab, CTLA-4-Ab, or a combination of PD-1-Ab and CTLA-4-Ab (PD-1/CTLA-4-Abs) were evaluated for ATAs at baseline and for thyroid function every 6 weeks for 24 weeks after treatment initiation and then observed until the last clinical visit. RESULTS: Of the 451 patients, 51 developed thyroid irAEs after immunotherapy [41 of 416 (9.9%) treated with PD-1-Ab, 0 of 8 (0%) treated with CTLA-4-Ab, and 10 of 27 (37.0%) treated with PD-1/CTLA-4-Abs]. The cumulative incidence of thyroid irAEs was significantly higher in patients who were positive vs negative for ATAs at baseline after both PD-1-Ab [28/87 (32.2%) vs 13/329 (4.0%), P < 0.001] and PD-1/CTLA-4-Abs [6/10 (60.0%) vs 4/17 (23.5%), P < 0.05] treatments. The risk of thyroid irAEs induced by PD-1/CTLA-4Abs, which was significantly higher than that induced by PD-1-Ab, in patients negative for ATAs at baseline was not statistically different from that induced by PD-1-Ab in patients positive for ATAs at baseline. CONCLUSIONS: This study showed that the incidence of thyroid irAEs was high and not negligible after PD-1/CTLA-4-Abs treatment even in patients negative for ATAs at baseline.

DOI： 10.1210/clinem/dgab829

Web of Science

PubMed

Functional lactotrophs in induced adenohypophysis differentiated from human iPS cells. Reviewed International journal

Natsuki Miyake, Takashi Nagai, Hidetaka Suga, Satoko Osuka, Takatoshi Kasai, Mayu Sakakibara, Mika Soen, Hajime Ozaki, Tsutomu Miwata, Tomoyoshi Asano, Mayuko Kano, Ayako Muraoka, Natsuki Nakanishi, Tomoko Nakamura, Maki Goto, Yoshinori Yasuda, Yohei Kawaguchi, Takashi Miyata, Tomoko Kobayashi, Mariko Sugiyama, Takeshi Onoue, Daisuke Hagiwara, Shintaro Iwama, Akira Iwase, Naoko Inoshita, Hiroshi Arima, Hiroaki Kajiyama

Endocrinology Vol. 163 ( 3 ) 2022.3

Language：English Publishing type：Research paper (scientific journal)

Prolactin (PRL), a hormone involved in lactation, is mainly produced and secreted by the lactotrophs of the anterior pituitary (AP) gland. We previously reported a method to generate functional adrenocorticotropic hormone-producing cells by differentiating the AP and hypothalamus simultaneously from human induced pluripotent stem cells (iPSCs). However, PRL-producing cells in the induced AP have not been investigated. Here, we confirmed the presence of PRL-producing cells and evaluated their endocrine functions. We differentiated pituitary cells from human iPSCs using serum-free floating culture of embryoid-like aggregates with quick reaggregation (SFEB-q) method and evaluated the appearance and function of PRL-producing cells. Secretion of PRL from the differentiated aggregates was confirmed, which increased with further culture. Fluorescence immunostaining and immunoelectron microscopy revealed PRL-producing cells and PRL-positive secretory granules, respectively. PRL secretion was promoted by various prolactin secretagogues such as thyrotropin-releasing hormone, vasoactive intestinal peptide, and prolactin-releasing peptide, and inhibited by bromocriptine. Moreover, the presence of tyrosine hydroxylase-positive dopaminergic nerves in the hypothalamic tissue area around the center of the aggregates connecting to PRL-producing cells indicated the possibility of recapitulating PRL regulatory mechanisms through the hypothalamus. In conclusion, we generated pituitary lactotrophs from human iPSCs; these displayed similar secretory responsiveness as human pituitary cells in vivo. In the future, this is expected to be used as a model of human PRL-producing cells for various studies, such as drug discovery, prediction of side effects, and elucidation of tumorigenic mechanisms using disease-specific iPSCs. Furthermore, it may help to develop regenerative medicine for the pituitary gland.

DOI： 10.1210/endocr/bqac004

Web of Science

PubMed

ヒト疾患特異的人工多能性幹細胞(iPS細胞)からのバソプレシン(AVP)神経の分化誘導による家族性中枢性尿崩症(FNDI)のin vitroヒト疾患モデル

尾崎創, 須賀英隆, 三輪田勤, 井口元三, 高橋裕, 有馬寛

日本内分泌学会雑誌 Vol. 97 ( 5 ) page： 1243 - 1243 2022.3

高脂肪食摂取に伴う中脳腹側被蓋野の炎症は絶食後の摂餌量を増加させる

孫汝楠, 杉山摩利子, 佐々木智之, 廣瀬友矩, 恒川卓, 高木博史, 坂野僚一, 有馬寛

肥満研究 Vol. 27 ( Suppl. ) page： 342 - 342 2022.3

Human Leukocyte Antigens and Biomarkers in Type Diabetes Mellitus Induced by Immune-Checkpoint Inhibitors

Inaba, H; Kaido, Y; Ito, S; Hirobata, T; Inoue, G; Sugita, T; Yamamoto, Y; Jinnin, M; Kimura, H; Kobayashi, T; Iwama, S; Arima, H; Matsuoka, T

ENDOCRINOLOGY AND METABOLISM Vol. 37 ( 1 ) page： 84 - + 2022.2

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Papers - ARIMA, Hiroshi