Faculty Profiles - ARIMA, Hiroshi

Papers - ARIMA, Hiroshi

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高脂肪食摂取により生じる視床下部弓状核と中脳腹側被蓋野の炎症は自発運動により抑制される

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

日本内分泌学会雑誌 Vol. 99 ( 1 ) page： 322 - 322 2023.5

木下珠希, 萩原大輔, 東慶成, 大山慎太郎, 有馬寛

日本内分泌学会雑誌 Vol. 99 ( 1 ) page： 293 - 293 2023.5

PD-1遮断における甲状腺機能障害のリスクはベースライン時の抗甲状腺抗体陽性数によって層別化される(The risk of thyroid dysfunction in PD-1 blockade is stratified by the number of positive anti-thyroid antibodies at baseline.)

Zhou Xin, 岩間信太郎, 小林朋子, 山上綾菜, 井土哲志, 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. 99 ( 1 ) page： 314 - 314 2023.5

抗PD-1抗体関連甲状腺機能異常症の臨床的特徴と抗甲状腺抗体価との関連

山上綾菜, 岩間信太郎, 小林朋子, Zhou Xin, 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. 99 ( 1 ) page： 306 - 306 2023.5

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メモリーT細胞分画、PD-1発現およびPD-L1発現の検討

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

日本内分泌学会雑誌 Vol. 99 ( 1 ) page： 305 - 305 2023.5

【甲状腺疾患アップデート:明日から役立つ最新知見】薬剤性甲状腺機能異常症抗PD-1抗体による甲状腺障害の基礎と臨床

安田康紀, 岩間信太郎, 有馬寛

診断と治療 Vol. 111 ( 5 ) page： 665 - 668 2023.5

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：(株)診断と治療社

＜文献概要＞Headline 1 免疫チェックポイント阻害薬(ICI)による免疫関連有害事象(irAE)の発症が問題となっており,内分泌irAEでは抗PD-1抗体による甲状腺障害の発症頻度が高い.2 抗PD-1抗体による甲状腺障害の発症には抗PD-1抗体治療開始前の甲状腺自己抗体の存在が発症リスク因子であり,発症機序として細胞傷害性CD4陽性T細胞から放出されるグランザイムBによる直接的な甲状腺組織傷害の関与が示唆されている.3 ICI治療を安全に継続するためには,ICI治療開始前での甲状腺自己抗体を含む甲状腺機能のフォローと内分泌専門医との連携が重要である.

Other Link： https://search.jamas.or.jp/default/link?pub_year=2023&ichushi_jid=J00697&link_issn=&doc_id=20230518020024&doc_link_id=10.34433%2Fdt.0000000264&url=https%3A%2F%2Fdoi.org%2F10.34433%2Fdt.0000000264&type=%E5%8C%BB%E6%9B%B8.jp_%E3%82%AA%E3%83%BC%E3%83%AB%E3%82%A2%E3%82%AF%E3%82%BB%E3%82%B9&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

Anti-tumor effects of anti-programmed cell death-1 antibody treatment are attenuated in streptozotocin-induced diabetic mice. Reviewed International journal

Masaaki Ito, Shintaro Iwama, Daisuke Sugiyama, Yoshinori Yasuda, Takayuki Okuji, Tomoko Kobayashi, Xin Zhou, Ayana Yamagami, Takeshi Onoue, Takashi Miyata, Mariko Sugiyama, Daisuke Hagiwara, Hidetaka Suga, Ryoichi Banno, Hiroyoshi Nishikawa, Hiroshi Arima

Scientific reports Vol. 13 ( 1 ) page： 5939 - 5939 2023.4

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

Hyperglycemia impairs immune response; however, it remains unknown whether the anti-tumor effects of anti-programmed cell death-1 antibody (PD-1-Ab) treatment are changed in hyperglycemic conditions. We analyzed the effect of PD-1-Ab on tumor growth in streptozotocin-induced diabetic mice (STZ-mice) subcutaneously inoculated with MC38 (a colon carcinoma cell line). Furthermore, we assessed the expression of chemokines by polymerase chain reaction (PCR) array in tumor-draining lymph nodes (dLNs) of these mice and MC38 cells cultured in different glucose concentrations. The suppressive effect of PD-1-Ab on tumor growth was attenuated. This was accompanied by fewer tumor-infiltrating CD8+ T cells, and STZ-mice had fewer tumor-infiltrating CD11c+ dendritic cells (DCs) than normoglycemic mice. mRNA expression levels of CXCL9, a chemokine recruiting CD8+ T cells, were lower in dLNs of STZ-mice than in normoglycemic mice after PD-1-Ab treatment, and its protein was expressed in DCs. In MC38 cells cultured with 25 mM glucose, mRNA expression of CCL7, a chemokine recruiting DCs, was decreased compared to cells cultured with 5 mM glucose. These results suggest that the STZ-induced hyperglycemia impairs the effect of PD-1-Ab treatment on MC38 tumor growth, and is accompanied by reduced infiltration of DCs and CD8+ T cells and decreased expression of CCL7 and CXCL9.

DOI： 10.1038/s41598-023-33049-7

Web of Science

PubMed

Generation of hypothalamic neural stem cell-like cells in vitro from human pluripotent stem cells. Reviewed International journal

Tsutomu Miwata, Hidetaka Suga, Yohei Kawaguchi, Mayu Sakakibara, Mayuko Kano, Shiori Taga, Mika Soen, Hajime Ozaki, Tomoyoshi Asano, Hiroo Sasaki, Takashi Miyata, Yoshinori Yasuda, Tomoko Kobayashi, Mariko Sugiyama, Takeshi Onoue, Hiroshi Takagi, Daisuke Hagiwara, Shintaro Iwama, Hiroshi Arima

Stem cell reports Vol. 18 ( 4 ) page： 869 - 883 2023.4

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

When damaged, restoring the function of the hypothalamus is currently impossible. It is unclear whether neural stem cells exist in the hypothalamus. Studies have reported that adult rodent tanycytes around the third ventricle function as hypothalamic neural stem cell-like cells. However, it is currently impossible to collect periventricular cells from humans. We attempted to generate hypothalamic neural stem cell-like cells from human embryonic stem cells (ESCs). We focused on retina and anterior neural fold homeobox (RAX) because its expression is gradually restricted to tanycytes during the late embryonic stage. We differentiated RAX::VENUS knockin human ESCs (hESCs) into hypothalamic organoids and sorted RAX+ cells from mature organoids. The isolated RAX+ cells formed neurospheres and exhibited self-renewal and multipotency. Neurogenesis was observed when neurospheres were transplanted into the mouse hypothalamus. We isolated RAX+ hypothalamic neural stem cell-like cells from wild-type human ES organoids. This is the first study to differentiate human hypothalamic neural stem cell-like cells from pluripotent stem cells.

DOI： 10.1016/j.stemcr.2023.02.006

Web of Science

PubMed

Amino acid polymorphisms in human histocompatibility leukocyte antigen class II and proinsulin epitope have impacts on type 1 diabetes mellitus induced by immune-checkpoint inhibitors Reviewed

Inaba, H; Morita, S; Kosugi, D; Asai, Y; Kaido, Y; Ito, S; Hirobata, T; Inoue, G; Yamamoto, Y; Jinnin, M; Kimura, H; Ota, M; Okudaira, Y; Nakatani, H; Kobayashi, T; Iwama, S; Arima, H; Matsuoka, T

FRONTIERS IN IMMUNOLOGY Vol. 14 page： 1165004 2023.4

Dapagliflozinは脂質と食塩の過剰摂取によって生じる耐糖能異常を改善する

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

糖尿病 Vol. 66 ( Suppl.1 ) page： S - 232 2023.4

Subcutaneous transplantation of human embryonic stem cells-derived pituitary organoids

Sasaki, H; Suga, H; Takeuchi, K; Nagata, Y; Harada, H; Kondo, T; Ito, E; Maeda, S; Sakakibara, M; Soen, M; Miwata, T; Asano, T; Ozaki, H; Taga, S; Kuwahara, A; Nakano, T; Arima, H; Saito, R

FRONTIERS IN ENDOCRINOLOGY Vol. 14 page： 1130465 2023.3

Resting energy expenditure depends on energy intake during weight loss in people with obesity: a retrospective cohort study. Reviewed International journal

Tomoko Handa, Takeshi Onoue, Tomoko Kobayashi, Eri Wada, Ayaka Hayase, Tamaki Kinoshita, Ayana Yamagami, Yoshinori Yasuda, Shintaro Iwama, Yohei Kawaguchi, Takashi Miyata, Mariko Sugiyama, Hiroshi Takagi, Daisuke Hagiwara, Hidetaka Suga, Ryoichi Banno, Motomitsu Goto, Hiroshi Arima

Archives of endocrinology and metabolism Vol. 67 ( 2 ) page： 233 - 241 2023.3

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

OBJECTIVE: Resting energy expenditure (REE) decreases if there is reduced energy intake and body weight (BW). The decrease in REE could make it difficult for patients with obesity to maintain decreased BW. This study aimed to investigate the correlation among changes in REE, energy intake, and BW during the weight loss process in patients with obesity. MATERIALS AND METHODS: We conducted a retrospective cohort study of patients hospitalized for the treatment of obesity in Japan. Patients received fully controlled diet during hospitalization and performed exercises if able. REE was measured once a week using a hand-held indirect calorimetry. Energy intake was determined by actual dietary intake. RESULTS: Of 44 inpatients with obesity, 17 were included in the analysis. Their BW decreased significantly after 1 week (-4.7 ± 2.0 kg, P < 0.001) and 2 weeks (-5.7 ± 2.2 kg, P < 0.001). The change in REE after 1 and 2 weeks was positively correlated with the energy intake/energy expenditure ratio (r = 0.66, P = 0.004 at 1 week, r = 0.71, P = 0.002 at 2 weeks). Using a regression equation (y = 0.5257x - 43.579), if the energy intake/energy expenditure ratio within the second week was 82.9%, the REE after 2 weeks was similar to the baseline level. There was no significant correlation between the change in REE and BW. CONCLUSION: Our data suggest that changes in REE depend on energy intake/energy expenditure ratio and that the decrease in REE can be minimized by matching energy intake to energy expenditure, even during the weight loss process.

DOI： 10.20945/2359-3997000000532

Web of Science

PubMed

抗PD-L1抗体による甲状腺障害の発症リスク因子の検討

小林朋子, 岩間信太郎, 山上綾菜, 周きん, 伊藤雅晃, 安田康紀, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 5 ) page： 1294 - 1294 2023.3

放射線治療とパシレオチドの併用が奏功したクッシング病の1例

村瀬萌絵, 安田康紀, 杉山摩利子, 永田雄一, 竹内和人, 井下尚子, 有馬寛

日本内分泌学会雑誌 Vol. 98 ( 5 ) page： 1401 - 1401 2023.3

Pyogenic spondylitis due to <i>Streptococcus agalactiae</i> with paraspinal abscess and vertebral destruction in a diabetic patient: time course of imagings Reviewed

Kobayashi, T; Iwata, T; Handa, K; Arima, H

ENDOCRINOLOGY DIABETES AND METABOLISM CASE REPORTS Vol. 2023 ( 1 ) 2023.1

Knockdown of endoplasmic reticulum chaperone BiP leads to the death of parvocellular AVP/CRH neurons in mice. Reviewed International journal

Yohei Kawaguchi, Daisuke Hagiwara, Tetsuro Tsumura, Takashi Miyata, Tomoko Kobayashi, Mariko Sugiyama, Takeshi Onoue, Yoshinori Yasuda, Shintaro Iwama, Hidetaka Suga, Ryoichi Banno, Valery Grinevich, Hiroshi Arima

Journal of neuroendocrinology Vol. 35 ( 1 ) page： e13223 2023.1

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

Arginine vasopressin (AVP) is expressed in both magnocellular (magnAVP) and parvocellular AVP (parvAVP) neurons of the paraventricular nucleus, and AVP colocalizes with corticotropin-releasing hormone (CRH) only in the parvocellular neurons. The immunoglobulin heavy chain binding protein (BiP) is a major endoplasmic reticulum (ER) chaperone which regulates the unfolded protein response under ER stress. We previously demonstrated that knockdown of BiP in magnAVP neurons exacerbated ER stress, which resulted in the autophagy-associated cell death of magnAVP neurons. Using the same approach, in the present study we examined the role of BiP in mouse parvAVP/CRH neurons. Our data demonstrate that BiP is expressed in mouse parvAVP/CRH neurons under nonstress conditions and is upregulated in proportion to the increase in CRH expression after adrenalectomy. For BiP knockdown in parvAVP/CRH neurons, we utilized a viral approach in combination with shRNA interference. Knockdown of BiP expression induced ER stress in parvAVP/CRH neurons, as reflected by the expression of C/EBP homologous protein. Furthermore, BiP knockdown led to the loss of parvAVP/CRH neurons after 4 weeks. In summary, our results demonstrate that BiP plays a pivotal role in parvAVP/CRH neurons, which function as neuroendocrine cells producing a large number of secretory proteins.

DOI： 10.1111/jne.13223

Web of Science

PubMed

Mineralocorticoids induce polyuria by reducing apical aquaporin-2 expression of the kidney in partial vasopressin deficiency.

Junki Kurimoto, Hiroshi Takagi, Takashi Miyata, Yohei Kawaguchi, Yuichi Hodai, Tetsuro Tsumura, Daisuke Hagiwara, Tomoko Kobayashi, Yoshinori Yasuda, Mariko Sugiyama, Takeshi Onoue, Shintaro Iwama, Hidetaka Suga, Ryoichi Banno, Takeshi Katsuki, Fumiaki Ando, Shinichi Uchida, Hiroshi Arima

Endocrine journal Vol. 70 ( 3 ) page： 295 - 304 2023

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

The symptoms of diabetes insipidus may be masked by the concurrence of adrenal insufficiency and emerge after the administration of hydrocortisone, occasionally at high doses. To elucidate the mechanism underlying polyuria induced by the administration of high-dose corticosteroids in the deficiency of arginine vasopressin (AVP), we first examined the secretion of AVP in three patients in whom polyuria was observed only after the administration of high-dose corticosteroids. Next, we examined the effects of dexamethasone or aldosterone on water balance in wild-type and familial neurohypophysial diabetes insipidus (FNDI) model mice. A hypertonic saline test showed that AVP secretion was partially impaired in all patients. In one patient, there were no apparent changes in AVP secretion before and after the administration of high-dose corticosteroids. In FNDI mice, unlike dexamethasone, the administration of aldosterone increased urine volumes and decreased urine osmolality. Immunohistochemical analyses showed that, after the administration of aldosterone in FNDI mice, aquaporin-2 expression was decreased in the apical membrane and increased in the basolateral membrane in the collecting duct. These changes were not observed in wild-type mice. The present data suggest that treatment with mineralocorticoids induces polyuria by reducing aquaporin-2 expression in the apical membrane of the kidney in partial AVP deficiency.

DOI： 10.1507/endocrj.EJ22-0339

Web of Science

PubMed

Response to endoplasmic reticulum stress in arginine vasopressin neurons. Invited

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

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

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

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

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Papers - ARIMA, Hiroshi