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Article ; Online: New perspectives on insulin therapy.

Araki, Eiichi / Araki, Hirotaka / Senokuchi, Takafumi / Motoshima, Hiroyuki

2020 Volume 11, Issue 4, Page(s) 795–797

MeSH term(s)	Diabetes Mellitus/drug therapy ; Glycemic Control/methods ; Glycemic Control/trends ; Humans ; Hypoglycemic Agents/therapeutic use ; Insulins/therapeutic use
Chemical Substances	Hypoglycemic Agents ; Insulins
Language	English
Publishing date	2020-05-21
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2625840-7
ISSN	2040-1124 ; 2040-1116
ISSN (online)	2040-1124
ISSN	2040-1116
DOI	10.1111/jdi.13263
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Article ; Online: Impacts of tight multifactorial intervention in patients with type 2 diabetes: Implications from the Japan Diabetes Outcome Intervention Trial 3.

Araki, Eiichi / Senokuchi, Takafumi / Furukawa, Noboru

Journal of diabetes investigation

2018 Volume 9, Issue 5, Page(s) 1022–1024

Abstract: Effects of intensive versus conventional therapy on the primary and secondary outcomes. ...

Abstract	Effects of intensive versus conventional therapy on the primary and secondary outcomes.
MeSH term(s)	Blood Glucose/drug effects ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/diagnosis ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/therapy ; Early Medical Intervention/methods ; Humans ; Hypoglycemic Agents/administration & dosage ; Japan/epidemiology ; Multicenter Studies as Topic/methods ; Randomized Controlled Trials as Topic/methods ; Treatment Outcome
Chemical Substances	Blood Glucose ; Hypoglycemic Agents
Language	English
Publishing date	2018-07-18
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	2625840-7
ISSN	2040-1124 ; 2040-1116
ISSN (online)	2040-1124
ISSN	2040-1116
DOI	10.1111/jdi.12872
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Article ; Online: Factors Affecting Human Damage in Heavy Rains and Typhoon Disasters.

Naito, Hisaki / Sueta, Daisuke / Hanatani, Satoko / Ikeda, Hatsuo / Hirosue, Akiyuki / Senokuchi, Takafumi / Araki, Eiichi / Tsujita, Kenichi / Nakayama, Hideki / Kasaoka, Shunji

The Tohoku journal of experimental medicine

2022 Volume 256, Issue 2, Page(s) 175–185

Abstract: Floods due to heavy rains or typhoons are frequent annual hazards in Japan. This study aims to reduce disaster fatalities and contribute to disaster risk reduction. This retrospective observational study analyzed fatalities caused by heavy rains or ... ...

Abstract	Floods due to heavy rains or typhoons are frequent annual hazards in Japan. This study aims to reduce disaster fatalities and contribute to disaster risk reduction. This retrospective observational study analyzed fatalities caused by heavy rains or typhoons. In Japan, 578 fatalities, related to seven occurrences of heavy rains and 16 typhoons, occurred between 2016 and 2020. Moreover, 13,195 houses collapsed due to hazards. Furthermore, 334 (73.2%) of the 456 fatalities were > 60 years old. Heavy rains caused more local area destruction due to floods and landslides than typhoons although wind- and disaster-related mortalities were found to be caused by typhoons. Human damage was eminent in older people because of their vulnerabilities and possibly dangerous behavior. Many fatalities were due to floods (46.9%) and landslides (44.1%). Indoor and outdoor mortalities due to heavy rains or typhoons were 157 (55.9%) and 124 (44.1%), respectively, and 24 (21.8%) of 124 outdoor mortalities occurred in vehicles. The number of recent flood mortalities in Japan correlates with the number of destroyed houses. Analyzing the victim's locations in the 2020 Kumamoto Heavy Rain using hazard and inundation maps suggested the difficulty of ensuring the safety of people living in dangerous areas. This study showed the characteristics of flood damage by heavy rains and typhoons in Japan and reports that flood damage is increasing because of the hazard size and community aging. Disaster risk reduction, disaster education, and evacuation safety plans for the elderly using hazard maps were important for strengthening disaster resilience.
MeSH term(s)	Aged ; Cyclonic Storms ; Disasters ; Floods ; Humans ; Japan/epidemiology ; Middle Aged ; Rain
Language	English
Publishing date	2022-03-02
Publishing country	Japan
Document type	Journal Article ; Observational Study
ZDB-ID	123477-8
ISSN	1349-3329 ; 0040-8727
ISSN (online)	1349-3329
ISSN	0040-8727
DOI	10.1620/tjem.256.175
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Article ; Online: Sirt7 Deficiency Attenuates Neointimal Formation Following Vascular Injury by Modulating Vascular Smooth Muscle Cell Proliferation.

Circulation journal : official journal of the Japanese Circulation Society

2021 Volume 85, Issue 12, Page(s) 2232–2240

Abstract: Background: Sirt7 is a recently identified sirtuin and has important roles in various pathological conditions, including cancer progression and metabolic disorders. It has previously been reported that Sirt7 is a key molecule in acute myocardial wound ... ...

Abstract	Background: Sirt7 is a recently identified sirtuin and has important roles in various pathological conditions, including cancer progression and metabolic disorders. It has previously been reported that Sirt7 is a key molecule in acute myocardial wound healing and pressure overload-induced cardiac hypertrophy. In this study, the role of Sirt7 in neointimal formation after vascular injury is investigated.Methods and Results:Systemic (Sirt7 Conclusions: Sirt7 deficiency attenuates neointimal formation after vascular injury. Given the predominant role in vascular neointimal formation, Sirt7 is a potentially suitable target for treatment of vascular diseases.
MeSH term(s)	Animals ; Cell Movement ; Cell Proliferation/physiology ; Cells, Cultured ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Neointima/pathology ; Sirtuins/genetics ; Sirtuins/metabolism ; Vascular System Injuries/genetics
Chemical Substances	SIRT7 protein, human ; Sirt7 protein, mouse ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2021-03-05
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2068090-9
ISSN	1347-4820 ; 1346-9843
ISSN (online)	1347-4820
ISSN	1346-9843
DOI	10.1253/circj.CJ-20-0936
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Article ; Online: Inhibition of inflammation-mediated DPP-4 expression by linagliptin increases M2 macrophages in atherosclerotic lesions.

Nishida, Shuhei / Matsumura, Takeshi / Senokuchi, Takafumi / Murakami-Nishida, Saiko / Ishii, Norio / Morita, Yutaro / Yagi, Yoshitaka / Motoshima, Hiroyuki / Kondo, Tatsuya / Araki, Eiichi

Biochemical and biophysical research communications

2020 Volume 524, Issue 1, Page(s) 8–15

Abstract: Background and aims: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, ... ...

Abstract	Background and aims: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage polarization in vitro and in vivo. Methods: Mouse bone marrow macrophages (BMMs) were used in in vitro assays. High fat diet (HFD)-fed Apoe Results: In in vitro assays using BMMs, treatment with LPS and IFNγ decreased the mRNA-expression levels of alternatively activated macrophage (M2) markers, and linagliptin treatment prevented these reductions. The mRNA levels of M2 markers and the number of M2 macrophages in the aorta were higher in linagliptin groups than in control groups. Linagliptin decreased the size of atherosclerotic lesions in HFD-fed Apoe Conclusions: Linagliptin increased M2 macrophage polarization by inhibiting DPP-4 expression and activity. These findings may indicate the beneficial effects of DPP-4 inhibitors on the progression of diabetic macrovascular complications.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/chemistry ; Anti-Inflammatory Agents/pharmacology ; Aorta/metabolism ; Atherosclerosis/drug therapy ; Bone Marrow Cells/drug effects ; Diet, High-Fat ; Dipeptidyl Peptidase 4/genetics ; Dipeptidyl Peptidase 4/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/chemistry ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Gene Expression Regulation/drug effects ; Humans ; Inflammation/drug therapy ; Linagliptin/chemistry ; Linagliptin/pharmacology ; Macrophages/cytology ; Macrophages/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Models, Animal ; RNA, Messenger/metabolism ; RNA, Small Interfering/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Dipeptidyl-Peptidase IV Inhibitors ; RNA, Messenger ; RNA, Small Interfering ; Linagliptin (3X29ZEJ4R2) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Language	English
Publishing date	2020-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.01.027
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Article: Study Design of a Phase II Clinical Trial to Assess the Efficacy and Safety of Eperisone in Japanese Type 2 Diabetes Patients with Risk and Non-risk Alleles of CDKAL1.

Sakakida, Kourin / Wei, Fan-Yan / Senokuchi, Takafumi / Shimoda, Seiya / Kakuma, Tatsuyuki / Araki, Eiichi / Tomizawa, Kazuhito

Acta medica Okayama

2018 Volume 72, Issue 4, Page(s) 423–426

Abstract: Genetic variation in Cdk5 Regulatory Associated Protein 1-Like 1 (CDKAL1) is associated with the development of type 2 diabetes (T2D). Dysfunction of CDKAL1 impairs the translation of proinsulin, which leads to glucose intolerance. Eperisone, an ... ...

Abstract	Genetic variation in Cdk5 Regulatory Associated Protein 1-Like 1 (CDKAL1) is associated with the development of type 2 diabetes (T2D). Dysfunction of CDKAL1 impairs the translation of proinsulin, which leads to glucose intolerance. Eperisone, an antispasmodic agent, has been shown to ameliorate glucose intolerance in Cdkal1-deficient mice. We have launched a phase II clinical study to investigate the potential anti-diabetic effect of eperisone in T2D patients carrying risk or non-risk alleles of CDKAL1. The primary endpoint is the change of hemoglobin A1c (HbA1c) levels. We also examined whether the efficacy of eperisone in T2D patients is associated with CDKAL1 activity.
MeSH term(s)	Adult ; Aged ; Alleles ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/genetics ; Glycated Hemoglobin A/analysis ; Humans ; Middle Aged ; Parasympatholytics/therapeutic use ; Propiophenones/adverse effects ; Propiophenones/therapeutic use ; Research Design ; Risk ; tRNA Methyltransferases/genetics
Chemical Substances	Glycated Hemoglobin A ; Parasympatholytics ; Propiophenones ; hemoglobin A1c protein, human ; eperisone (2M2P0551D3) ; tRNA Methyltransferases (EC 2.1.1.-) ; CDKAL1 protein, human (EC 2.8.4.5)
Language	English
Publishing date	2018-08-23
Publishing country	Japan
Document type	Clinical Trial ; Clinical Trial, Phase II ; Journal Article
ZDB-ID	188415-3
ISSN	0386-300X ; 0001-6152
ISSN	0386-300X ; 0001-6152
DOI	10.18926/AMO/56182
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Article ; Online: Impact of tissue macrophage proliferation on peripheral and systemic insulin resistance in obese mice with diabetes.

Morita, Yutaro / Senokuchi, Takafumi / Yamada, Sarie / Wada, Toshiaki / Furusho, Tatsuya / Matsumura, Takeshi / Ishii, Norio / Nishida, Saiko / Nishida, Syuhei / Motoshima, Hiroyuki / Komohara, Yoshihiro / Yamagata, Kazuya / Araki, Eiichi

BMJ open diabetes research & care

2020 Volume 8, Issue 1

Abstract: Introduction: Obesity-related insulin resistance is a widely accepted pathophysiological feature in type 2 diabetes. Systemic metabolism and immunity are closely related, and obesity represents impaired immune function that predisposes individuals to ... ...

Abstract	Introduction: Obesity-related insulin resistance is a widely accepted pathophysiological feature in type 2 diabetes. Systemic metabolism and immunity are closely related, and obesity represents impaired immune function that predisposes individuals to systemic chronic inflammation. Increased macrophage infiltration and activation in peripheral insulin target tissues in obese subjects are strongly related to insulin resistance. Using a macrophage-specific proliferation inhibition mouse model (mac-p27Tg), we previously reported that suppressed plaque inflammation reduced atherosclerosis and improved plaque stabilization. However, the direct evidence that proliferating macrophages are responsible for inducing insulin resistance was not provided. Research design and methods: The mac-p27Tg mice were fed a high-fat diet, and glucose metabolism, histological changes, macrophage polarization, and tissue functions were investigated to reveal the significance of tissue macrophage proliferation in insulin resistance and obesity. Results: The mac-p27Tg mice showed improved glucose tolerance and insulin sensitivity, along with a decrease in the number and ratio of inflammatory macrophages. Obesity-induced inflammation and oxidative stress was attenuated in white adipose tissue, liver, and gastrocnemius. Histological changes related to insulin resistance, such as liver steatosis/fibrosis, adipocyte enlargement, and skeletal muscle fiber transformation to fast type, were ameliorated in mac-p27Tg mice. Serum tumor necrosis factor alpha and free fatty acid were decreased, which might partially impact improved insulin sensitivity and histological changes. Conclusions: Macrophage proliferation in adipose tissue, liver, and skeletal muscle was involved in promoting the development of systemic insulin resistance. Controlling the number of tissue macrophages by inhibiting macrophage proliferation could be a therapeutic target for insulin resistance and type 2 diabetes.
MeSH term(s)	Animals ; Cell Proliferation ; Diabetes Mellitus, Type 2/complications ; Insulin Resistance ; Macrophages ; Mice ; Mice, Obese
Language	English
Publishing date	2020-09-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732918-5
ISSN	2052-4897 ; 2052-4897
ISSN (online)	2052-4897
ISSN	2052-4897
DOI	10.1136/bmjdrc-2020-001578
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Article ; Online: Pioglitazone suppresses macrophage proliferation in apolipoprotein-E deficient mice by activating PPARγ.

Murakami-Nishida, Saiko / Matsumura, Takeshi / Senokuchi, Takafumi / Ishii, Norio / Kinoshita, Hiroyuki / Yamada, Sarie / Morita, Yutaro / Nishida, Shuhei / Motoshima, Hiroyuki / Kondo, Tatsuya / Komohara, Yoshihiro / Araki, Eiichi

Atherosclerosis

2019 Volume 286, Page(s) 30–39

Abstract: Background and aims: Local macrophage proliferation is linked to enhanced atherosclerosis progression. Our previous study found that troglitazone, a thiazolidinedione (TZD), suppressed oxidized low-density lipoprotein (Ox-LDL)-induced macrophage ... ...

Abstract	Background and aims: Local macrophage proliferation is linked to enhanced atherosclerosis progression. Our previous study found that troglitazone, a thiazolidinedione (TZD), suppressed oxidized low-density lipoprotein (Ox-LDL)-induced macrophage proliferation. However, its effects and mechanisms are unclear. Therefore, we investigated the effects of pioglitazone, another TZD, on macrophage proliferation. Methods: Normal chow (NC)- or high-fat diet (HFD)-fed apolipoprotein E-deficient (Apoe Results: Atherosclerosis progression was suppressed in aortic sinuses of pioglitazone-treated Apoe Conclusions: Pioglitazone suppressed macrophage proliferation through PPARγ without inducing macrophage apoptosis. These findings imply that pioglitazone could prevent macrovascular complications in diabetic individuals.
MeSH term(s)	Animals ; Apolipoproteins E/deficiency ; Atherosclerosis/prevention & control ; Cell Proliferation/drug effects ; Macrophages/cytology ; Macrophages/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; PPAR gamma/physiology ; Pioglitazone/pharmacology ; Pioglitazone/therapeutic use
Chemical Substances	Apolipoproteins E ; PPAR gamma ; Pioglitazone (X4OV71U42S)
Language	English
Publishing date	2019-05-03
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2019.04.229
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Article: Inhibition of inflammation-mediated DPP-4 expression by linagliptin increases M2 macrophages in atherosclerotic lesions

Nishida, Shuhei / Matsumura, Takeshi / Senokuchi, Takafumi / Murakami-Nishida, Saiko / Ishii, Norio / Morita, Yutaro / Yagi, Yoshitaka / Motoshima, Hiroyuki / Kondo, Tatsuya / Araki, Eiichi

Biochemical and biophysical research communications. 2020 Mar. 26, v. 524, no. 1

2020

Abstract: Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage ... ...

Abstract	Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to suppress atherosclerosis progression in atherosclerotic mouse models through unclear mechanisms. In this study, we investigated the effect of the DPP-4 inhibitor, linagliptin, on macrophage polarization in vitro and in vivo.Mouse bone marrow macrophages (BMMs) were used in in vitro assays. High fat diet (HFD)-fed Apoe⁻/⁻ mice were treated orally with linagliptin (10 mg/kg⁻¹•day⁻¹) or a vehicle (water) control.In in vitro assays using BMMs, treatment with LPS and IFNγ decreased the mRNA-expression levels of alternatively activated macrophage (M2) markers, and linagliptin treatment prevented these reductions. The mRNA levels of M2 markers and the number of M2 macrophages in the aorta were higher in linagliptin groups than in control groups. Linagliptin decreased the size of atherosclerotic lesions in HFD-fed Apoe⁻/⁻ mice. Interestingly, inflammatory stimulation increased DPP-4 expression, and linagliptin suppressed these effects in BMMs. Treatment with DPP-4 small-interfering RNA (siRNA) reproduced linagliptin-mediated alteration of M2 polarization.Linagliptin increased M2 macrophage polarization by inhibiting DPP-4 expression and activity. These findings may indicate the beneficial effects of DPP-4 inhibitors on the progression of diabetic macrovascular complications.
Keywords	aorta ; atherosclerosis ; bone marrow ; high fat diet ; macrophages ; mice ; research
Language	English
Dates of publication	2020-0326
Size	p. 8-15.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.01.027
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Article ; Online: Hepatocellular carcinoma development in diabetic patients: a nationwide survey in Japan.

Tateishi, Ryosuke / Matsumura, Takeshi / Okanoue, Takeshi / Shima, Toshihide / Uchino, Koji / Fujiwara, Naoto / Senokuchi, Takafumi / Kon, Kazuyoshi / Sasako, Takayoshi / Taniai, Makiko / Kawaguchi, Takumi / Inoue, Hiroshi / Watada, Hirotaka / Kubota, Naoto / Shimano, Hitoshi / Kaneko, Shuichi / Hashimoto, Etsuko / Watanabe, Sumio / Shiota, Goshi /

Ueki, Kohjiro / Kashiwabara, Kosuke / Matsuyama, Yutaka / Tanaka, Hideo / Kasuga, Masato / Araki, Eiichi / Koike, Kazuhiko

Journal of gastroenterology

2021 Volume 56, Issue 3, Page(s) 261–273

Abstract: Background: Although type 2 diabetes mellitus (T2DM) is a known risk factor for hepatocellular carcinoma (HCC) development, the annual incidence in diabetes patients is far below the threshold of efficient surveillance. This study aimed to elucidate the ...

Abstract	Background: Although type 2 diabetes mellitus (T2DM) is a known risk factor for hepatocellular carcinoma (HCC) development, the annual incidence in diabetes patients is far below the threshold of efficient surveillance. This study aimed to elucidate the risk factors for HCC in diabetic patients and to determine the best criteria to identify surveillance candidates. Methods: The study included 239 patients with T2DM who were diagnosed with non-viral HCC between 2010 and 2015, with ≥ 5 years of follow-up at diabetes clinics of 81 teaching hospitals in Japan before HCC diagnosis, and 3277 non-HCC T2DM patients from a prospective cohort study, as controls. Clinical data at the time of and 5 years before HCC diagnosis were collected. Results: The mean patient age at HCC diagnosis was approximately 73 years, and 80% of the patients were male. The proportion of patients with insulin use increased, whereas the body mass index (BMI), proportion of patients with fatty liver, fasting glucose levels, and hemoglobin A1c (HbA1c) levels decreased significantly in 5 years. In the cohort study, 18 patients developed HCC during the mean follow-up period of 4.7 years with an annual incidence of 0.11%. Multivariate logistic regression analyses showed that the FIB-4 index was an outstanding predictor of HCC development along with male sex, presence of hypertension, lower HbA1c and albumin levels, and higher BMI and gamma-glutamyl transpeptidase levels. Receiver-operating characteristic analyses showed that a FIB-4 cut-off value of 3.61 could help identify high-risk patients, with a corresponding annual HCC incidence rate of 1.1%. Conclusion: A simple calculation of the FIB-4 index in diabetes clinics can be the first step toward surveillance of HCC with a non-viral etiology.
MeSH term(s)	Aged ; Carcinoma, Hepatocellular/etiology ; Carcinoma, Hepatocellular/physiopathology ; Cohort Studies ; Diabetes Complications/etiology ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/physiopathology ; Female ; Humans ; Japan/epidemiology ; Liver Neoplasms/epidemiology ; Liver Neoplasms/etiology ; Liver Neoplasms/physiopathology ; Logistic Models ; Male ; Middle Aged ; ROC Curve ; Registries/statistics & numerical data ; Surveys and Questionnaires
Language	English
Publishing date	2021-01-11
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1186495-3
ISSN	1435-5922 ; 0944-1174
ISSN (online)	1435-5922
ISSN	0944-1174
DOI	10.1007/s00535-020-01754-z
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