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Article ; Online: TYK2 signaling promotes the development of autoreactive CD8

Mine, Keiichiro / Nagafuchi, Seiho / Akazawa, Satoru / Abiru, Norio / Mori, Hitoe / Kurisaki, Hironori / Shimoda, Kazuya / Yoshikai, Yasunobu / Takahashi, Hirokazu / Anzai, Keizo

Nature communications

2024 Volume 15, Issue 1, Page(s) 1337

Abstract: Tyrosine kinase 2 (TYK2), a member of the JAK family, has attracted attention as a potential therapeutic target for autoimmune diseases. However, the role of TYK2 in ... ...

Abstract	Tyrosine kinase 2 (TYK2), a member of the JAK family, has attracted attention as a potential therapeutic target for autoimmune diseases. However, the role of TYK2 in CD8
MeSH term(s)	Mice ; Animals ; CD8-Positive T-Lymphocytes ; T-Lymphocytes, Cytotoxic ; Diabetes Mellitus, Type 1/genetics ; TYK2 Kinase/genetics ; Mice, Knockout ; Mice, Inbred NOD ; Antineoplastic Agents
Chemical Substances	TYK2 Kinase (EC 2.7.10.2) ; Antineoplastic Agents
Language	English
Publishing date	2024-02-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45573-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: SARS-CoV-2 Infection and Pancreatic β Cell Failure.

Mine, Keiichiro / Nagafuchi, Seiho / Mori, Hitoe / Takahashi, Hirokazu / Anzai, Keizo

Biology

2021 Volume 11, Issue 1

Abstract: SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 ... ...

Abstract	SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 infection may also be a causal factor for diabetes mellitus in patients with COVID-19. According to the research reviewed in this paper, the pancreas and pancreatic β cells appear to be targets of SARS-CoV-2 and are damaged by direct or indirect effects of the infection. However, controversial results have been reported between study groups, mainly due to the limited number of cases with diabetes precipitated by COVID-19. In this review, we comprehensively discuss the published findings on the potential association between SARS-CoV-2 infection or COVID-19 and pancreatic β-cell damage leading to diabetes onset. These findings will further contribute to our understanding of the pathogenesis of diabetes mellitus.
Language	English
Publishing date	2021-12-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11010022
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Article: [A case of repeated severe hypoglycemia caused by accidental ingestion of sulfonylurea in an elderly patient].

Yamasaki, Arina / Imazono, Naohiro / Iwano, Ayane / Kishikawa, Mariko / Inoue, Akira / Mori, Hitoe / Takeichi, Yukina / Kojima, Motoyasu / Anzai, Keizo

Nihon Ronen Igakkai zasshi. Japanese journal of geriatrics

2023 Volume 60, Issue 3, Page(s) 294–300

Abstract: An 81-year-old man was being treated with oral medication for chronic heart failure and epilepsy. He had no history of diabetes, cirrhosis, or gastric surgery. He was admitted to our hospital due to disturbance of consciousness. His blood glucose level ... ...

Abstract	An 81-year-old man was being treated with oral medication for chronic heart failure and epilepsy. He had no history of diabetes, cirrhosis, or gastric surgery. He was admitted to our hospital due to disturbance of consciousness. His blood glucose level was 6 mg/dl, with a relatively high insulin level (14.4 μU/ml). Computed tomography and a 48 h fasting test showed no signs of insulinoma. There were no signs of reactive hypoglycemia, insulin autoimmune syndrome, or adrenal insufficiency. His wife had been taking medication for diabetes, including sulfonylurea. She had dementia, and he managed her medication. Since his medication was found in his wife's medicine box, we considered the possibility that he might have taken sulfonylurea by mistake. We asked his daughter to manage their medicine. However, one month later, he was admitted to our hospital again with severe hypoglycemia. His wife's HbA1c value and estimated glomerular filtration rate were 6.9% and 30 ml/min/1.73 m
MeSH term(s)	Humans ; Aged ; Male ; Female ; Aged, 80 and over ; Glycated Hemoglobin ; Hypoglycemia/chemically induced ; Insulin ; Pancreatic Neoplasms ; Eating
Chemical Substances	Glycated Hemoglobin ; Insulin
Language	Japanese
Publishing date	2023-09-20
Publishing country	Japan
Document type	Case Reports ; English Abstract ; Journal Article
ZDB-ID	604107-3
ISSN	0300-9173
ISSN	0300-9173
DOI	10.3143/geriatrics.60.294
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Article: SARS-CoV-2 Infection and Pancreatic β Cell Failure

Mine, Keiichiro / Nagafuchi, Seiho / Mori, Hitoe / Takahashi, Hirokazu / Anzai, Keizo

Biology. 2021 Dec. 24, v. 11, no. 1

2021

Abstract	SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 infection may also be a causal factor for diabetes mellitus in patients with COVID-19. According to the research reviewed in this paper, the pancreas and pancreatic β cells appear to be targets of SARS-CoV-2 and are damaged by direct or indirect effects of the infection. However, controversial results have been reported between study groups, mainly due to the limited number of cases with diabetes precipitated by COVID-19. In this review, we comprehensively discuss the published findings on the potential association between SARS-CoV-2 infection or COVID-19 and pancreatic β-cell damage leading to diabetes onset. These findings will further contribute to our understanding of the pathogenesis of diabetes mellitus.
Keywords	COVID-19 infection ; Severe acute respiratory syndrome coronavirus 2 ; diabetes mellitus ; pathogenesis ; risk factors
Language	English
Dates of publication	2021-1224
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology11010022
Database	NAL-Catalogue (AGRICOLA)

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Article: Genetic Susceptibility of the Host in Virus-Induced Diabetes

Mine, Keiichiro / Yoshikai, Yasunobu / Takahashi, Hirokazu / Mori, Hitoe / Anzai, Keizo / Nagafuchi, Seiho

Microorganisms. 2020 July 27, v. 8, no. 8

2020

Abstract: Enteroviruses, especially Coxsackie B viruses, are among the candidate environmental factors causative of type 1 diabetes. Host genetic factors have an impact on the development of virus-induced diabetes (VID). Host background, in terms of whether the ... ...

Abstract	Enteroviruses, especially Coxsackie B viruses, are among the candidate environmental factors causative of type 1 diabetes. Host genetic factors have an impact on the development of virus-induced diabetes (VID). Host background, in terms of whether the host is prone to autoimmunity, should also be considered when analyzing the role of target genes in VID. In this review, we describe the genetic susceptibility of the host based on studies in humans and VID animal models. Understanding the host genetic factors should contribute not only to revealing the mechanisms of VID development, but also in taking measures to prevent VID.
Keywords	Enterovirus ; animal models ; autoimmunity ; environmental factors ; genes ; genetic factors ; humans ; insulin-dependent diabetes mellitus ; viruses
Language	English
Dates of publication	2020-0727
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8081133
Database	NAL-Catalogue (AGRICOLA)

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Article: Genetic Susceptibility of the Host in Virus-Induced Diabetes.

Mine, Keiichiro / Yoshikai, Yasunobu / Takahashi, Hirokazu / Mori, Hitoe / Anzai, Keizo / Nagafuchi, Seiho

Microorganisms

2020 Volume 8, Issue 8

Abstract	Enteroviruses, especially Coxsackie B viruses, are among the candidate environmental factors causative of type 1 diabetes. Host genetic factors have an impact on the development of virus-induced diabetes (VID). Host background, in terms of whether the host is prone to autoimmunity, should also be considered when analyzing the role of target genes in VID. In this review, we describe the genetic susceptibility of the host based on studies in humans and VID animal models. Understanding the host genetic factors should contribute not only to revealing the mechanisms of VID development, but also in taking measures to prevent VID.
Language	English
Publishing date	2020-07-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8081133
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Impaired upregulation of Stat2 gene restrictive to pancreatic β-cells is responsible for virus-induced diabetes in DBA/2 mice

Mine, Keiichiro / Nagafuchi, Seiho / Hatano, Shinya / Tanaka, Kenichi / Mori, Hitoe / Takahashi, Hirokazu / Anzai, Keizo / Yoshikai, Yasunobu

Biochemical and biophysical research communications. 2020 Jan. 22, v. 521, no. 4

2020

Abstract: Viral infection is a putative causal factor for the development of type 1 diabetes, but the exact pathogenic mechanism of virus-induced diabetes (VID) remains unclear. Here, to identify the critical factors that regulate VID, we analyzed ... ...

Abstract	Viral infection is a putative causal factor for the development of type 1 diabetes, but the exact pathogenic mechanism of virus-induced diabetes (VID) remains unclear. Here, to identify the critical factors that regulate VID, we analyzed encephalomyocarditis D (EMC-D) VID-sensitive DBA/2 mice in comparison with resistant B6 mice. EMC-D virus-induced cell death occurred more frequently in DBA/2 β-cells than in B6 β-cells with 100U/ml IFN-β priming in vitro. We therefore purified β-cells using flow cytometry from mice two days after EMC-D virus infection and subjected them to microarray analysis. As a results, innate immune response pathway was found to be enriched in B6 β-cells. The signal transducer and activator of transcription 2 (Stat2) gene interacted with genes in the pathway. Stat2 gene expression levels were lower in DBA/2 mice than in B6 mice, restrictive to β-cells. Moreover, administration of IFN-β failed to upregulate Stat2 gene in DBA/2 β-cells than in those of B6 in vivo. The viral titer significantly increased only in the DBA/2 pancreas. Thus, these provided data suggest that impaired upregulation of Stat2 gene restrictive to β-cells at the early stage of infection is responsible for VID development in DBA/2 mice.
Keywords	cell death ; flow cytometry ; gene expression ; genes ; innate immunity ; insulin-dependent diabetes mellitus ; microarray technology ; research ; signal transduction ; transactivators ; viral load ; viruses
Language	English
Dates of publication	2020-0122
Size	p. 853-860.
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.2019.10.193
Database	NAL-Catalogue (AGRICOLA)

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Article: TYK2 Promoter Variant Is Associated with Impaired Insulin Secretion and Lower Insulin Resistance in Japanese Type 2 Diabetes Patients

Mori, Hitoe / Takahashi, Hirokazu / Mine, Keiichiro / Higashimoto, Ken / Inoue, Kanako / Kojima, Motoyasu / Kuroki, Shigetaka / Eguchi, Takahisa / Ono, Yasuhiro / Inuzuka, Sadataka / Soejima, Hidenobu / Nagafuchi, Seiho / Anzai, Keizo

Genes. 2021 Mar. 11, v. 12, no. 3

2021

Abstract: Accumulating evidence has suggested that viral infection causes type 1 diabetes due to direct β-cell damage and the triggering of autoimmune reactivity to β cells. Here, we elucidated that the tyrosine kinase 2 (Tyk2) gene, encoding an interferon ... ...

Abstract	Accumulating evidence has suggested that viral infection causes type 1 diabetes due to direct β-cell damage and the triggering of autoimmune reactivity to β cells. Here, we elucidated that the tyrosine kinase 2 (Tyk2) gene, encoding an interferon receptor signaling molecule, is responsible for virus-induced diabetes in mice, and its promoter variant confers a risk of type 1 diabetes in humans. This study investigated the relationship between a TYK2 promoter variant (TYK2PV) and insulin secretion in type 2 diabetes patients. TYK2PV status was determined using direct DNA sequencing and its associations with fasting insulin, C-peptide, and homeostatic model assessment of insulin resistance (HOMA-IR) were evaluated in type 2 diabetes patients without sulfonylurea or insulin medication. Of the 172 patients assessed, 18 (10.5%) showed TYK2PV-positivity. Their body mass index (BMI) was significantly lower than in those without the variant (23.4 vs. 25.4 kg/m², p = 0.025). Fasting insulin (3.9 vs. 6.2 μIU/mL, p = 0.007), C-peptide (1.37 vs. 1.76 ng/mL, p = 0.008), and HOMA-IR (1.39 vs. 2.05, p = 0.006) were lower in those with than in those without the variant. Multivariable analysis identified that TYK2PV was associated with fasting insulin ≤ 5 μIU/mL (odds ratio (OR) 3.63, p = 0.025) and C-peptide ≤ 1.0 ng/mL (OR 3.61, p = 0.028), and also lower insulin resistance (HOMA-IR ≤ 2.5; OR 8.60, p = 0.042). TYK2PV is associated with impaired insulin secretion and low insulin resistance in type 2 diabetes. Type 2 diabetes patients with TYK2PV should be carefully followed in order to receive the appropriate treatment including insulin injections.
Keywords	DNA ; body mass index ; c-peptide ; drug therapy ; genes ; insulin resistance ; insulin secretion ; insulin-dependent diabetes mellitus ; interferons ; noninsulin-dependent diabetes mellitus ; odds ratio ; risk ; tyrosine
Language	English
Dates of publication	2021-0311
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12030400
Database	NAL-Catalogue (AGRICOLA)

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Article: Administration of Jerusalem artichoke reduces the postprandial plasma glucose and glucose-dependent insulinotropic polypeptide (GIP) concentrations in humans.

Takahashi, Hirokazu / Nakajima, Akane / Matsumoto, Yuichi / Mori, Hitoe / Inoue, Kanako / Yamanouchi, Hiroko / Tanaka, Kenichi / Tomiga, Yuki / Miyahara, Maki / Yada, Tomomi / Iba, Yumiko / Matsuda, Yayoi / Watanabe, Keiichi / Anzai, Keizo

Food & nutrition research

2022 Volume 66

Abstract: Background: The consumption of Jerusalem artichoke has multiple beneficial effects against diabetes and obesity.: Objective: The aim of this study was to determine the effect of a single administration of Jerusalem artichoke tubers on postprandial ... ...

Abstract	Background: The consumption of Jerusalem artichoke has multiple beneficial effects against diabetes and obesity. Objective: The aim of this study was to determine the effect of a single administration of Jerusalem artichoke tubers on postprandial glycemia and the concentrations of incretin hormones in humans. Method: Grated Jerusalem artichoke was administered prior to a meal (Trial 1; white rice for prediabetic participants, Results: Jerusalem artichoke significantly reduced the glucose and GIP concentrations after the consumption of either meal in Trial 1 and Trial 3, whereas there were no differences in the insulin, glucagon, and active GLP-1 concentrations. Also, there was no significant difference in the triglyceride concentration after the ingestion of the fat-rich meal in Trial 3. The glucose and GIP-lowering effects were dose-dependent, and the consumption of at least 100 g of Jerusalem artichoke was required to have these effects in Trial 2. Conclusion: This study demonstrates that a single administration of Jerusalem artichoke tubers reduces postprandial glucose and active GIP concentrations in prediabetic and healthy individuals.
Language	English
Publishing date	2022-04-04
Publishing country	Sweden
Document type	Journal Article
ZDB-ID	2418338-6
ISSN	1654-661X ; 1654-661X ; 1654-6628
ISSN (online)	1654-661X
ISSN	1654-661X ; 1654-6628
DOI	10.29219/fnr.v66.7870
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Article ; Online: HSPA8

Genes

2022 Volume 13, Issue 7

Abstract: There is an association between nonalcoholic fatty liver disease (NAFLD) and atherosclerosis, but the genetic risk of atherosclerosis in NAFLD remains unclear. Here, a single-nucleotide polymorphism (SNP) of the heat shock 70 kDa protein 8 ( ...

Abstract	There is an association between nonalcoholic fatty liver disease (NAFLD) and atherosclerosis, but the genetic risk of atherosclerosis in NAFLD remains unclear. Here, a single-nucleotide polymorphism (SNP) of the heat shock 70 kDa protein 8 (
MeSH term(s)	Humans ; Male ; Atherosclerosis/genetics ; Carotid Arteries ; Carotid Artery Diseases/genetics ; Carotid Intima-Media Thickness ; HSC70 Heat-Shock Proteins ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/genetics ; Polymorphism, Single Nucleotide
Chemical Substances	HSC70 Heat-Shock Proteins ; HSPA8 protein, human
Language	English
Publishing date	2022-07-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13071265
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