論文 - 神津　英至

Independent Link Between Use of Mineralocorticoid Receptor Antagonists and Muscle Wasting in Heart Failure Patients Not Receiving Renin-Angiotensin System Inhibitors

Ryo Numazawa, Satoshi Katano, Toshiyuki Yano, Ryohei Nagaoka, Katsuhiko Ohori, Hidemichi Kouzu, Suguru Honma, Yusuke Fujisawa, Kotaro Yamano, Arata Osanami, Masayuki Koyama, Akiyoshi Hashimoto, Masato Furuhashi

Circulation Journal ( Japanese Circulation Society )   2023年10月

DOI

Optimal serum 25-hydroxyvitamin D level to prevent sarcopenia in patients with heart failure: insights from a dose-response relationship

Ryohei Nagaoka, Satoshi Katano, Toshiyuki Yano, Ryo Numazawa, Kotaro Yamano, Yusuke Fujisawa, Suguru Honma, Tatsuki Kamoda, Kohei Sato, Hidemichi Kouzu, Katsuhiko Ohori, Masaki Katayose, Akiyoshi Hashimoto, Masato Furuhashi

Nutrition, Metabolism and Cardiovascular Diseases ( Elsevier BV )   2023年10月

DOI

Circulating level of β-aminoisobutyric acid (BAIBA), a novel myokine-like molecule, is inversely associated with fat mass in patients with heart failure

Satoshi Katano, Toshiyuki Yano, Hidemichi Kouzu, Ryohei Nagaoka, Ryo Numazawa, Kotaro Yamano, Yusuke Fujisawa, Katsuhiko Ohori, Nobutaka Nagano, Takefumi Fujito, Ryo Nishikawa, Wataru Ohwada, Masaki Katayose, Tatsuya Sato, Atsushi Kuno, Masato Furuhashi

Heart and Vessels ( Springer Science and Business Media LLC )   2023年09月

DOI

心不全患者におけるレニン-アンジオテンシン系活性化は骨格筋量の低下と関連する

沼澤 瞭, 片野 唆敏, 矢野 俊之, 長岡 凌平, 神津 英至, 大堀 克彦, 藤澤 佑輔, 山埜 光太郎, 長南 新太, 小山 雅之, 橋本 暁佳, 古橋 眞人

日本高血圧学会総会プログラム・抄録集 ( (NPO)日本高血圧学会 )  45回   398 - 398  2023年09月

Development and validation of osteoporosis risk assessment score, ORAS, in heart failure patients: comparison with the Osteoporosis Self-Assessment Tool for Asians (OSTA)

Ryo Numazawa, Satoshi Katano, Toshiyuki Yano, Masayuki Koyama, Ryohei Nagaoka, Yusuke Fujisawa, Kotaro Yamano, Suguru Honma, Katsuhiko Ohori, Hidemichi Kouzu, Masaki Katayose, Masato Furuhashi, Kazufumi Tsuchihashi, Akiyoshi Hashimoto

European Journal of Cardiovascular Nursing ( Oxford University Press (OUP) )   2023年08月

　概要を見る

Abstract Aim Osteoporosis is prevalent and is associated with poor prognosis in heart failure (HF) patients. However, bone mineral density (BMD) measurement by a dual-energy X-ray absorptiometry (DEXA) scan is not always available in a daily clinical setting and large-scale population-based studies. Methods A single-center, cross-sectional observational study was conducted with 387 patients (median age: 77 years [interquartile range: 68 to 83 years]; 37% women). BMDs were measured by DEXA scans, and osteoporosis was diagnosed as ≤ -2.5 standard deviation of the BMDs in healthy young adults. Osteoporosis risk assessment score (ORAS) was developed using significant predictors from a logistic regression model for osteoporosis and was subsequently validated. Results Osteoporosis was found in 103 (27%) of the 387 HF patients. Multivariate logistic regression analyses yielded the ORAS based on sex, BMI, handgrip strength, and anti-coagulant therapy utilization. The C-index of ORAS in the developmental set (0.796, 95% confidence interval: 0.747 to 0.845) was similar to the bootstrap validation of the prediction model (0.784), and tended to be higher than that of the Osteoporosis Self-Assessment Tool for Asians (OSTA). A nomogram of ORAS, established on the basis of the final logistic regression model, demonstrated 100% sensitivity at the lowest score (35 points), with an optimal cutoff point of 127 points, yielding 85% sensitivity and 62% specificity. Conclusions ORAS exhibits superior predictive performance to OSTA in predicting osteoporosis in HF patients, establishing itself as a valuable tool for early detection in both daily clinical practice and large-scale population-based studies.

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Impact of Radar Chart-Based Information Sharing in a Multidisciplinary Team on In-Hospital Outcomes and Prognosis in Older Patients With Heart Failure

Satoshi Katano, Toshiyuki Yano, Ryo Numazawa, Ryohei Nagaoka, Kotaro Yamano, Yusuke Fujisawa, Suguru Honma, Ayako Watanabe, Katsuhiko Ohori, Hidemichi Kouzu, Takefumi Fujito, Tomoyuki Ishigo, Hayato Kunihara, Hiroya Fujisaki, Masaki Katayose, Akiyoshi Hashimoto, Masato Furuhashi

Circulation Reports ( Japanese Circulation Society )   2023年06月

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Independent Association Between Use of Proton Pump Inhibitors and Muscle Wasting in Patients with Heart Failure: A Single-Center, Ambispective, Observational Study

Katsuhiko Ohori, Toshiyuki Yano, Satoshi Katano, Ryohei Nagaoka, Ryo Numazawa, Kotaro Yamano, Yusuke Fujisawa, Hidemichi Kouzu, Masayuki Koyama, Nobutaka Nagano, Takefumi Fujito, Ryo Nishikawa, Wataru Ohwada, Masato Furuhashi

Drugs & Aging ( Springer Science and Business Media LLC )   2023年06月

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Early Commencement and Long-Term Continuation of Tolvaptan Treatment Attenuate Functional Impairment of Renal Vasopressin V2 Receptors and Improve Clinical Outcomes in Patients with Heart Failure

Takahiro Noto, Arata Osanami, Nobutaka Nagano, Nobuaki Kokubu, Hidemichi Kouzu, Masaya Tanno

International Heart Journal ( International Heart Journal (Japanese Heart Journal) )  64 ( 1 ) 36 - 43  2023年03月

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Downregulation of BCKDH Activity and Uncoupling from AMP Deaminase Underlie Substrate Inflexibility in Type 2 Diabetic Hearts(タイトル和訳中)

小川 俊史, 神津 英至, 長南 新太, 清水 将輝, 戸田 悠貴, 大和田 渉, 佐藤 達也, 矢野 俊之, 久野 篤史, 丹野 雅也, 三浦 哲嗣, 古橋 眞人

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  87回   OJ03 - 2  2023年03月

BCKDH活性のダウンレギュレーションとAMPデアミナーゼとのアンカップリングが2型糖尿病性心臓における基質柔軟性の欠如を引き起こす(Downregulation of BCKDH Activity and Uncoupling from AMP Deaminase Underlie Substrate Inflexibility in Type 2 Diabetic Hearts)

小川 俊史, 神津 英至, 長南 新太, 清水 将輝, 戸田 悠貴, 大和田 渉, 佐藤 達也, 矢野 俊之, 久野 篤史, 丹野 雅也, 三浦 哲嗣, 古橋 眞人

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  87回   OJ03 - 2  2023年03月

Impact of Iron Metabolism on Physical Function in Patients with Heart Failure(タイトル和訳中)

大堀 克彦, 矢野 俊之, 片野 唆敏, 長岡 凌平, 沼澤 瞭, 山埜 光太郎, 藤沢 祐輔, 神津 英至, 小山 雅之, 永野 伸卓, 藤戸 健史, 西川 諒, 大和田 渉, 古橋 眞人

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  87回   PJ038 - 3  2023年03月

心不全患者の骨粗鬆症を予測する新たなリスクスコアの開発と精度の検証

沼澤 瞭, 片野 唆敏, 長岡 凌平, 藤澤 佑輔, 山埜 光太郎, 大堀 克彦, 渡辺 絢子, 石郷 友之, 西川 諒, 大和田 渉, 永野 伸卓, 藤戸 健史, 小山 雅之, 神津 英至, 橋本 暁佳, 矢野 俊之, 古橋 眞人

日本循環器学会学術集会抄録集 ( (一社)日本循環器学会 )  87回   CA1 - 2  2023年03月

Adenosine monophosphate deaminase in the endoplasmic reticulum-mitochondria interface promotes mitochondrial Ca2+ overload in type 2 diabetes rat hearts.

Arata Osanami, Tatsuya Sato, Yuki Toda, Masaki Shimizu, Atsushi Kuno, Hidemichi Kouzu, Toshiyuki Yano, Wataru Ohwada, Toshifumi Ogawa, Tetsuji Miura, Masaya Tanno

Journal of diabetes investigation    2023年02月  [国内誌]

　概要を見る

AIMS/INTRODUCTION: We previously showed that upregulation of myocardial adenosine monophosphate deaminase (AMPD) is associated with pressure overload-induced diastolic dysfunction in type 2 diabetes hearts. Here, we examined involvement of AMPD localized in the endoplasmic reticulum-mitochondria interface in mitochondrial Ca2+ overload and its pathological significance. MATERIALS AND METHODS: We used type 2 diabetes Otsuka Long-Evans Tokushima Fatty rats (OLETF) and non-diabetes Long-Evans Tokushima Otsuka Fatty rats (LETO) as well as AMPD3-overexpressing H9c2 cells and human embryonic kidney 293 cells. RESULTS: OLETF, but not LETO, showed diastolic dysfunction under the condition of phenylephrine-induced pressure overload. The levels of 90-kDa AMPD3 in outer mitochondrial membranes/endoplasmic reticulum and mitochondria-associated endoplasmic reticulum membrane (MAM) fractions were significantly higher in OLETF than in LETO. The area of the MAM quantified by electron microscopic analysis was 57% larger, mitochondrial Ca2+ level under the condition of pressure overload was 47% higher and Ca2+ retention capacity in MAM-containing crude mitochondria isolated before the pressure overloading was 21% lower in OLETF than in LETO (all P-values <0.05). Transfection of FLAG-AMPD3 in cells resulted in significant enlargement of the MAM area, and impairment in pyruvate/malate-driven adenosine triphosphate-stimulated and uncoupler-stimulated mitochondrial respiration compared with those in control cells. CONCLUSIONS: The findings suggest that 90-kDa AMPD3 localized in the endoplasmic reticulum-mitochondria interface promotes formation of the MAM, inducing mitochondrial Ca2+ overload and dysfunction in type 2 diabetes hearts.

DOI PubMed

Downregulation of extramitochondrial BCKDH and its uncoupling from AMP deaminase in type 2 diabetic OLETF rat hearts

Toshifumi Ogawa, Hidemichi Kouzu, Arata Osanami, Yuki Tatekoshi, Tatsuya Sato, Atsushi Kuno, Yugo Fujita, Shoya Ino, Masaki Shimizu, Yuki Toda, Wataru Ohwada, Toshiyuki Yano, Masaya Tanno, Takayuki Miki, Tetsuji Miura

Physiological Reports   11 ( 4 ) e15608  2023年02月  [査読有り]  [国際誌]

　概要を見る

Systemic branched-chain amino acid (BCAA) metabolism is dysregulated in cardiometabolic diseases. We previously demonstrated that upregulated AMP deaminase 3 (AMPD3) impairs cardiac energetics in a rat model of obese type 2 diabetes, Otsuka Long-Evans-Tokushima fatty (OLETF). Here, we hypothesized that the cardiac BCAA levels and the activity of branched-chain α-keto acid dehydrogenase (BCKDH), a rate-limiting enzyme in BCAA metabolism, are altered by type 2 diabetes (T2DM), and that upregulated AMPD3 expression is involved in the alteration. Performing proteomic analysis combined with immunoblotting, we discovered that BCKDH localizes not only to mitochondria but also to the endoplasmic reticulum (ER), where it interacts with AMPD3. Knocking down AMPD3 in neonatal rat cardiomyocytes (NRCMs) increased BCKDH activity, suggesting that AMPD3 negatively regulates BCKDH. Compared with control rats (Long-Evans Tokushima Otsuka [LETO] rats), OLETF rats exhibited 49% higher cardiac BCAA levels and 49% lower BCKDH activity. In the cardiac ER of the OLETF rats, BCKDH-E1α subunit expression was downregulated, while AMPD3 expression was upregulated, resulting in an 80% lower AMPD3-E1α interaction compared to LETO rats. Knocking down E1α expression in NRCMs upregulated AMPD3 expression and recapitulated the imbalanced AMPD3-BCKDH expressions observed in OLETF rat hearts. E1α knockdown in NRCMs inhibited glucose oxidation in response to insulin, palmitate oxidation, and lipid droplet biogenesis under oleate loading. Collectively, these data revealed previously unrecognized extramitochondrial localization of BCKDH in the heart and its reciprocal regulation with AMPD3 and imbalanced AMPD3-BCKDH interactions in OLETF. Downregulation of BCKDH in cardiomyocytes induced profound metabolic changes that are observed in OLETF hearts, providing insight into mechanisms contributing to the development of diabetic cardiomyopathy.

DOI PubMed

Nuclear translocation of MLKL enhances necroptosis by a RIP1/RIP3-independent mechanism in H9c2 cardiomyoblasts.

Shoya Ino, Toshiyuki Yano, Atsushi Kuno, Masaya Tanno, Hidemichi Kouzu, Tatsuya Sato, Tomohisa Yamashita, Wataru Ohwada, Arata Osanami, Toshifumi Ogawa, Yuki Toda, Masaki Shimizu, Tetsuji Miura

Journal of pharmacological sciences   151 ( 2 ) 134 - 143  2023年02月  [国内誌]

　概要を見る

Accumulating evidence suggests that necroptosis of cardiomyocytes contributes to cardiovascular diseases. Lethal disruption of the plasma membrane in necroptosis is induced by oligomers of mixed lineage kinase domain-like (MLKL) that is translocated to the membrane from the cytosol. However, the role played by cytoplasmic-nuclear shuttling of MLKL is unclear. Here, we tested the hypothesis that translocation of MLKL to the nucleus promotes the necroptosis of cardiomyocytes. Activation of the canonical necroptotic signaling pathway by a combination of TNF-α and zVAD (TNF/zVAD) increased nuclear MLKL levels in a RIP1-activity-dependent manner in H9c2 cells, a rat cardiomyoblast cell line. By use of site-directed mutagenesis, we found a nuclear export signal sequence in MLKL and prepared its mutant (MLKL-L280/283/284A), though a search for a nuclear import signal was unsuccessful. MLKL-L280/283/284A localized to both the cytosol and the nucleus. Expression of MLKL-L280/283/284A induced necroptotic cell death, which was attenuated by GppNHp, an inhibitor of Ran-mediated nuclear import, but not by inhibition of RIP1 activity or knockdown of RIP3 expression. GppNHp partly suppressed H9c2 cell death induced by TNF/zVAD treatment. These results suggest that MLKL that is translocated to the nucleus via RIP1-mediated necroptotic signaling enhances the necroptosis of cardiomyocytes through a RIP1-/RIP3-independent mechanism.

DOI PubMed

Case report: Transient lactate elevation by intravenous insulin infusion therapy for diabetic ketoacidosis in a patient with mitochondrial DNA 3243 A > G mutation: A glycolysis rebooting syndrome?

Wataru Ohwada, Hidemichi Kouzu, Tatsuya Sato, Kahomi Sazawa, Azumi Matsui, Nobutaka Nagano, Masayuki Koyama, Noriko Ogasawara, Akifumi Takada, Toshiyuki Yano, Masato Furuhashi

Frontiers in cardiovascular medicine   10   1144925 - 1144925  2023年  [国際誌]

　概要を見る

Mitochondrial disease, most cases of which are caused by mitochondrial DNA (mtDNA) mutation, is present with multiple phenotypes including diabetes mellitus, sensorineural hearing loss, cardiomyopathy, muscle weakness, renal dysfunction, and encephalopathy, depending on the degree of heteroplasmy. While mitochondria play an important role in intracellular glucose and lactate metabolism in insulin-sensitive tissues such as muscles, appropriate strategies for glycemic control have not yet been established in a patient with mitochondrial disease, which is often complicated by myopathy. Here, we describe the history of a 40-year-old man with mtDNA 3243A > G who had sensorineural hearing loss, cardiomyopathy, muscle wasting, and diabetes mellitus with stage 3 chronic kidney disease. He developed mild diabetic ketoacidosis (DKA) in the process of treatment for poor glycemic control with severe latent hypoglycemia. According to the standard therapy for DKA, he was treated with continuous intravenous insulin infusion therapy, which unexpectedly resulted in an abrupt and transient elevation in blood lactate levels without exacerbation of heart failure and kidney function. Since blood lactate levels are determined by the balance between lactate production and consumption, an abrupt and transient lactate elevation following intravenous insulin injection therapy may reflect not only enhanced glycolysis in insulin-sensitive tissues with mitochondrial dysfunction but also decreased lactate consumption in the sarcopenic skeletal muscle and failing heart. Intravenous insulin infusion therapy in patients with mitochondrial disease may unmask derangements of intracellular glucose metabolism in response to insulin signaling.

DOI PubMed

Potential favorable action of sodium-glucose cotransporter-2 inhibitors on sudden cardiac death: a brief overview.

Tatsuya Sato, Hidemichi Kouzu, Toshiyuki Yano, Ichiro Sakuma, Masato Furuhashi, Noritsugu Tohse

Frontiers in cardiovascular medicine   10   1159953 - 1159953  2023年  [国際誌]

　概要を見る

The primary pharmacological action of sodium-glucose co-transporter 2 (SGLT2) inhibitors is to inhibit the reabsorption of glucose and sodium ions from the proximal tubules of the kidney and to promote urinary glucose excretion. Notably, several clinical trials have recently demonstrated potent protective effects of SGLT2 inhibitors in patients with heart failure (HF) or chronic kidney disease (CKD), regardless of the presence or absence of diabetes. However, the impact of SGLT2 inhibitors on sudden cardiac death (SCD) or fatal ventricular arrhythmias (VAs), the pathophysiology of which is partly similar to that of HF and CKD, remains undetermined. The cardiorenal protective effects of SGLT2 inhibitors have been reported to include hemodynamic improvement, reverse remodeling of the failing heart, amelioration of sympathetic hyperactivity, correction of anemia and impaired iron metabolism, antioxidative effects, correction of serum electrolyte abnormalities, and antifibrotic effects, which may lead to prevent SCD and/or VAs. Recently, as possible direct cardiac effects of SGLT2 inhibitors, not only inhibition of Na+/H+ exchanger (NHE) activity, but also suppression of late Na+ current have been focused on. In addition to the indirect cardioprotective mechanisms of SGLT2 inhibitors, suppression of aberrantly increased late Na+ current may contribute to preventing SCD and/or VAs via restoration of the prolonged repolarization phase in the failing heart. This review summarizes the results of previous clinical trials of SGLT2 inhibitors for prevention of SCD, their impact on the indices of electrocardiogram, and the possible molecular mechanisms of their anti-arrhythmic effects.

DOI PubMed

Loss of perceived social role, an index of social frailty, is an independent predictor of future adverse events in hospitalized patients with heart failure

Ayako Watanabe, Satoshi Katano, Toshiyuki Yano, Ryohei Nagaoka, Ryo Numazawa, Suguru Honma, Kotaro Yamano, Yusuke Fujisawa, Katsuhiko Ohori, Hidemichi Kouzu, Tomoyuki Ishigo, Masaki Katayose, Akiyoshi Hashimoto, Masato Furuhashi

Frontiers in Cardiovascular Medicine ( Frontiers Media SA )  9  2022年12月

　概要を見る

Aims Although the impact of physical frailty on prognosis and the effect of cardiac rehabilitation in HF patients has been well established, data for the prognostic impact of social frailty (SF) in HF patients are limited. In addition, the relative importance of each SF domain in clinical outcomes remains unclear. We aimed to get a new insight into the associations of SF with clinical outcomes in elderly hospitalized HF patients. Methods A single-center, retrospective cohort study was conducted using data from 310 in-hospital HF patients aged ≥ 65 years (mean age of 78 ± 8 years; 49% women). Makizako’s five questions, a self-reported questionnaire, were used to define SF. The primary outcome was composite events defined by all-cause death and cardiovascular events. Results Of the 310 elderly HF patients, 188 patients (61%) had SF. Seventy-five patients (24%) had composite events during a mean follow-up period of 1.93 ± 0.91 years. Kaplan-Meier curves showed that patients with SF had a significantly higher composite event rate than patients without SF. In multivariate Cox regression analyses, SF was independently associated with a higher composite event rate after adjusting for prognostic markers [adjusted hazard ratio (HR), 2.01; 95% confidence interval (CI), 1.07–3.78; p = 0.04]. Of the 5 questions for defining SF, an answer of yes to the question about not feeling helpful toward friends or family, which indicates loss of perceived social role, was an independent predictor of composite events (adjusted HR, 2.28; 95% CI, 1.36–3.82; p &lt; 0.01). Inclusion of loss of perceived social role into the baseline prognostic model improved both the continuous net reclassification improvement (0.562; 95% CI, 0.298–0.827; p &lt; 0.01) and integrated discrimination improvement (0.031; 95% CI, 0.006–0.056; p = 0.02). Conclusion Loss of perceived social role is associated with increased adverse event risk and provides additive prognostic information in elderly HF patients.

DOI

Elevated circulating level of β-aminoisobutyric acid (BAIBA) in heart failure patients with type 2 diabetes receiving sodium-glucose cotransporter 2 inhibitors

Satoshi Katano, Toshiyuki Yano, Hidemichi Kouzu, Ryohei Nagaoka, Ryo Numazawa, Kotaro Yamano, Yusuke Fujisawa, Katsuhiko Ohori, Nobutaka Nagano, Takefumi Fujito, Ryo Nishikawa, Wataru Ohwada, Masaki Katayose, Tatsuya Sato, Atsushi Kuno, Masato Furuhashi

Cardiovascular Diabetology ( Springer Science and Business Media LLC )  21 ( 1 )  2022年12月

　概要を見る

Abstract Aims The mechanism by which a sodium-glucose cotransporter inhibitor (SGLT2i) induces favorable effects on diabetes and cardiovascular diseases including heart failure (HF) remains poorly understood. Metabolomics including amino acid profiling enables detection of alterations in whole body metabolism. The aim of this study was to determine whether plasma amino acid profiles are modulated by SGLT2i use in HF patients with type 2 diabetes mellitus (T2DM). Methods We retrospectively examined 81 HF patients with T2DM (68 ± 11 years old; 78% male). Plasma amino acid concentrations in a fasting state after stabilization of HF were determined using ultraperformance liquid chromatography. To minimize potential selection bias in the retrospective analyses, the differences in baseline characteristics between patients receiving an SGLT2i and patients not receiving an SGLT2i were controlled by using an inverse probability of treatment weighting (IPTW)-adjusted analysis. Results Of amino acids measurable in the present assay, plasma β-aminoisobutyric acid (BAIBA), an exercise-induced myokine-like molecule also known as 3-aminoisobutyric acid or 3-amino-2-methyproponic acid, was detected in 77% of all patients and the proportion of patients in whom plasma BAIBA was detected was significantly higher in patients receiving an SGLT2i than in patients not receiving an SGLT2i (93% vs. 67%, p = 0.01). Analyses in patients in whom plasma BAIBA was detected showed that plasma BAIBA concentration was significantly higher in patients receiving an SGLT2i than in patients not receiving an SGLT2i (6.76 ± 4.72 vs. 4.56 ± 2.93 nmol/ml, p = 0.03). In multivariate logistic regression analyses that were adjusted for age and sex, SGLT2i use was independently associated with BAIBA detection. The independent association between BAIBA and SGLT2i use remained after inclusion of body mass index, HF with reduced ejection fraction, ischemic etiology, renal function, NT-proBNP, albumin, hemoglobin, and HbA1c into the Cox proportional hazards model. When the differences in baseline characteristics between patients receiving an SGLT2i and patients not receiving an SGLT2i were controlled by using an IPTW-adjusted analysis, least squares mean of plasma BAIBA concentration was significantly higher in patients receiving an SGLT2i than in patients not receiving an SGLT2i. Conclusion SGLT2i use is closely associated with increased circulating BAIBA concentration in HF patients with T2DM.

DOI

治療中に乳酸値上昇を呈したミトコンドリア糖尿病に合併したケトアシドーシスの1例

佐澤 佳穂実, 大和田 渉, 馬場 周平, 柏柳 杏美, 小松 弘明, 永野 伸卓, 小山 雅之, 佐藤 達也, 神津 英至, 小笠原 徳子, 矢野 俊之

糖尿病 ( (一社)日本糖尿病学会 )  65 ( 10 ) 552 - 552  2022年10月