Faculty Profiles - ARIMA, Hiroshi

Papers - ARIMA, Hiroshi

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Response to endoplasmic reticulum stress in arginine vasopressin neurons. Invited Open Access

Daisuke Hagiwara, Yoshinori Azuma, Yohei Kawaguchi, Takashi Miyata, Hiroshi Arima

Endocrine journal Vol. 70 ( 6 ) page： 567 - 572 2023

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

Arginine vasopressin (AVP) is an antidiuretic hormone synthesized principally in the hypothalamic supraoptic and paraventricular nuclei. The immunoglobulin heavy chain binding protein (BiP), one of the most abundant endoplasmic reticulum (ER) chaperones, is highly expressed in AVP neurons, even under basal conditions. Moreover, its expression is upregulated in proportion to the increase in AVP expression under dehydration. These data suggest that AVP neurons are constantly exposed to ER stress. BiP knockdown in AVP neurons induces ER stress and autophagy, resulting in AVP neuronal loss, indicating that BiP is pivotal in maintaining the AVP neuron system. Furthermore, inhibition of autophagy after BiP knockdown exacerbates AVP neuronal loss, suggesting that autophagy induced under ER stress is a protective cellular mechanism by which AVP neurons cope with ER stress. Familial neurohypophysial diabetes insipidus (FNDI) is an autosomal dominant disorder caused by mutations in the AVP gene. It is characterized by delayed-onset progressive polyuria and eventual AVP neuronal loss. In AVP neurons of FNDI model mice, mutant protein aggregates are confined to a specific compartment of the ER, called the ER-associated compartment (ERAC). The formation of ERACs contributes to maintaining the function of the remaining intact ER, and mutant protein aggregates in ERACs undergo autophagic-lysosomal degradation without isolation or translocation from the ER, representing a novel protein degradation system in the ER.

DOI： 10.1507/endocrj.EJ23-0193

Open Access

Web of Science

PubMed

A retrospective study on tolvaptan prescription in clinical practice in patients with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) using the Japanese claims database Reviewed Open Access

Hagiwara, D; Matsukawa, M; Tasaki, J; Nakamura, Y; Arima, H

ENDOCRINE JOURNAL Vol. 70 ( 12 ) page： 1195 - 1205 2023

Changing the Name of Diabetes Insipidus: A Position Statement of the Working Group for Renaming Diabetes Insipidus. Reviewed Open Access

Arima H, Cheetham T, Christ-Crain M, Cooper D, Drummond J, Gurnell M, Levy M, McCormack A, Newell-Price J, Verbalis JG, Wass J, Working Group for Renaming Diabetes Insipidus

The Journal of clinical endocrinology and metabolism Vol. 108 ( 1 ) page： 1 - 3 2022.12

Changing the name of diabetes insipidus

Arima, H; Bichet, DG; Cheetham, T; Christ-Crain, M; Drummond, J; Gurnell, M; Levy, M; McCormack, A; Newell-Price, J; Verbalis, JG; Wass, J; Cooper, D

PITUITARY Vol. 25 ( 6 ) page： 777 - 779 2022.12

Changing the name of diabetes insipidus: a position statement of The Working Group for Renaming Diabetes Insipidus. Open Access

Working Group for Renaming Diabetes Insipidus, Arima H, Cheetham T, Christ-Crain M, Cooper D, Gurnell M, Drummond JB, Levy M, McCormack AI, Verbalis J, Newell-Price J, Wass JAH

Endocrine journal Vol. 69 ( 11 ) page： 1281 - 1284 2022.11

Changing the name of diabetes insipidus: a position statement of The Working Group for Renaming Diabetes Insipidus Open Access

Arima, H; Cheetham, T; Christ-Crain, M; Cooper, D; Gurnell, M; Drummond, JB; Levy, M; McCormack, AI; Verbalis, J; Newell-Price, J; Wass, JAH

ENDOCRINE CONNECTIONS Vol. 11 ( 11 ) 2022.11

Changing the name of diabetes insipidus: a position statement of The Working Group for Renaming Diabetes Insipidus Open Access

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

EUROPEAN JOURNAL OF ENDOCRINOLOGY Vol. 187 ( 5 ) page： P1 - P3 2022.11

Changing the name of diabetes insipidus: a position statement of the working group to consider renaming diabetes insipidus Open Access

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

ARCHIVES OF ENDOCRINOLOGY METABOLISM Vol. 66 ( 6 ) page： 868 - 870 2022.11

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. International journal Open Access

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

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

Open Access

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 Open Access

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 Open Access

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 Open Access

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

Open Access

Web of Science

PubMed

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

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 Open Access

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 Open Access

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

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Papers - ARIMA, Hiroshi