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  1. Article ; Online: Possible etiological role of impaired endogenous double strand RNA editing in β-cells in type 1 diabetes.

    Imai, Junta

    Journal of diabetes investigation

    2024  

    Abstract: Proposed mechanisms by which disruption of endogenous dsRNA editing in β-cells leads to type 1 diabetes-like phenotypes in βAdarKO mice. Disruption of endogenous dsRNA editing in β-cells initiates IFN responses, thereby inducing pancreatic islet ... ...

    Abstract Proposed mechanisms by which disruption of endogenous dsRNA editing in β-cells leads to type 1 diabetes-like phenotypes in βAdarKO mice. Disruption of endogenous dsRNA editing in β-cells initiates IFN responses, thereby inducing pancreatic islet inflammation and β-cell dysfunction. Hyperglycemia induced by β-cell dysfunction further promotes islet inflammation, likely via increased dsRNA resulting from increased β-cell workload, thereby producing a vicious cycle. The mechanism by which impairment of dsRNA editing is integrated with autoimmune-mediated pathogenesis of type 1 diabetes remains to be clarified.
    Language English
    Publishing date 2024-04-25
    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.14224
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    Zs.A 6920: Show issues Location:
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  2. Article ; Online: Identification of islet cell characteristics in humans with type 2 diabetes by single-cell sequencing.

    Imai, Junta

    Journal of diabetes investigation

    2022  Volume 13, Issue 10, Page(s) 1646–1648

    Abstract: Pathologically, type 2 diabetes mellitus develops on the basis of insufficient insulin action. Insulin action insufficiency results from impaired insulin secretion and/or insulin resistance, i.e., the failure of insulin to exert sufficient effects. ... ...

    Abstract Pathologically, type 2 diabetes mellitus develops on the basis of insufficient insulin action. Insulin action insufficiency results from impaired insulin secretion and/or insulin resistance, i.e., the failure of insulin to exert sufficient effects. Impairment of insulin secretion is attributable to an insufficient pancreatic β cell mass and/or pancreatic β cell dysfunction, features collectively referred to as β cell failure. As β cell failure plays a critical role in the pathology of type 2 diabetes, strategies aimed at reversing β cell failure or preserving β cells before failure becomes evident are urgently needed. However, difficulties in conducting experiments on pancreatic β cells in vivo, especially in humans, are a major challenge impeding the development of such eagerly-awaited therapeutic options. In a recent Journal of Clinical Investigation article, Son et al. described their efforts to identify an alteration in regulatory protein activity in human β cells, which is elicited in the state of type 2 diabetes, and explored therapeutic options for preventing β cell failure.
    MeSH term(s) Diabetes Mellitus, Type 2/drug therapy ; Humans ; Insulin/therapeutic use ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Islets of Langerhans/metabolism
    Chemical Substances Insulin
    Language English
    Publishing date 2022-06-04
    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.13833
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  3. Article ; Online: Regulation of Adaptive Cell Proliferation by Vagal Nerve Signals for Maintenance of Whole-Body Homeostasis: Potential Therapeutic Target for Insulin-Deficient Diabetes.

    Imai, Junta

    The Tohoku journal of experimental medicine

    2021  Volume 254, Issue 4, Page(s) 245–252

    Abstract: In insulin-resistant states such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. Failure of this β-cells proliferative response leads to the development of diabetes. On the other hand, when organs are damaged, cells ... ...

    Abstract In insulin-resistant states such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. Failure of this β-cells proliferative response leads to the development of diabetes. On the other hand, when organs are damaged, cells proliferate to repair the organs. Therefore, these proliferations are compensatory mechanisms aimed at maintaining whole-body homeostasis. We previously discovered vagal signal-mediated systems regulating adaptive proliferation of β-cells and hepatocytes. Neuron-mediated liver-β-cell inter-organ crosstalk is involved in promotion of β-cell proliferation during obesity, and in this system, vagal signals directly stimulate β-cell proliferation. Meanwhile, in the liver, the multi-step mechanisms whereby vagal nerve signals activate hepatic resident macrophages are involved in hepatocyte proliferation after severe injury. Diabetes mellitus develops on the pathological basis of insufficient insulin action. Insulin action insufficiency is attributable to insulin resistance, i.e., the failure of insulin to exert sufficient effects, and/or to impairment of insulin secretion. Impairment of insulin secretion is attributable not only to the β-cell dysfunction but also to functional β-cell mass reduction. In this regard, there are already therapeutic options to increase insulin secretion from residual β-cells, such as sulfonyl urea and incretin-related drugs. In contrast, there are as yet no applicable therapeutic strategies to increase functional β-cell mass in vivo. Therefore, we have conducted the basic investigations to tackle this issue based on the discovery of neuron-mediated liver-β-cell inter-organ crosstalk. This review introduces vagal signal-mediated regulatory systems of adaptive cell proliferation in vivo and efforts to develop cell-increasing therapies based on vagal nerve-mediated cell proliferation.
    MeSH term(s) Cell Proliferation ; Diabetes Mellitus, Type 2 ; Homeostasis ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism
    Chemical Substances Insulin
    Language English
    Publishing date 2021-08-07
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 123477-8
    ISSN 1349-3329 ; 0040-8727
    ISSN (online) 1349-3329
    ISSN 0040-8727
    DOI 10.1620/tjem.254.245
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  4. Article ; Online: β-Cell senescence in the pathogenesis of type 2 diabetes.

    Imai, Junta

    Journal of diabetes investigation

    2019  Volume 11, Issue 2, Page(s) 284–286

    Abstract: The prevalence of type 2 diabetes increases with aging, and the type 2 diabetes developing in the elderly is often accompanied by a gradual impairment of β-cell function and reduced β-cell mass along with aging. However, the contribution of β-cell ... ...

    Abstract The prevalence of type 2 diabetes increases with aging, and the type 2 diabetes developing in the elderly is often accompanied by a gradual impairment of β-cell function and reduced β-cell mass along with aging. However, the contribution of β-cell senescence to the pathogenesis of type 2 diabetes remains uncertain. In a recent Cell Metabolism article, Aguayo-Mazzucato et al. described their efforts to identify the signatures of senescent β-cells, and explored the role(s) of senescent β-cells in type 2 diabetes.
    MeSH term(s) Aging/physiology ; Animals ; Cellular Senescence/physiology ; Diabetes Mellitus, Type 2/physiopathology ; Disease Models, Animal ; Humans ; Insulin Resistance/physiology ; Insulin-Secreting Cells/physiology ; Mice
    Language English
    Publishing date 2019-11-19
    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.13162
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  5. Article ; Online: Regulation of compensatory β-cell proliferation by inter-organ networks from the liver to pancreatic β-cells.

    Imai, Junta

    Endocrine journal

    2018  Volume 65, Issue 7, Page(s) 677–684

    Abstract: In insulin-resistant states such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. However, the mechanism(s) by which obesity induces compensatory β-cell responses is not fully understood. Recently, several studies have ... ...

    Abstract In insulin-resistant states such as obesity, pancreatic β-cells proliferate to prevent blood glucose elevations. However, the mechanism(s) by which obesity induces compensatory β-cell responses is not fully understood. Recently, several studies have shown that signals from the liver, such as neuronal signals or humoral factors, regulate β-cell proliferation during obesity development. We previously reported a liver-brain-pancreas neuronal relay, consisting of afferent splanchnic nerves, the central nervous system and efferent vagal nerves, to promote this compensatory β-cell proliferation. Furthermore, we recently clarified the molecular mechanisms by which efferent vagal signals induce β-cell proliferation in this inter-organ neuronal network system. Herein, these liver-β-cell inter-organ networks are reviewed, focusing mainly on the neuronal network. The significance of the neuronal network system in the maintenance of glucose homeostasis is also discussed with reference to the relevant literature.
    MeSH term(s) Cell Proliferation/physiology ; Humans ; Insulin-Secreting Cells/physiology ; Liver/innervation ; Liver/physiology ; Neural Pathways/physiology ; Neurons/physiology ; Pancreas/innervation ; Pancreas/physiology
    Language English
    Publishing date 2018-07-03
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 1151918-6
    ISSN 1348-4540 ; 0918-8959
    ISSN (online) 1348-4540
    ISSN 0918-8959
    DOI 10.1507/endocrj.EJ18-0241
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  6. Article ; Online: Insulin allergy manifesting soon after COVID-19 vaccination (BNT162b2).

    Komamura, Hiroshi / Kawana, Yohei / Imai, Junta / Katagiri, Hideki

    Journal of diabetes investigation

    2022  Volume 14, Issue 3, Page(s) 498–499

    Abstract: We experienced a case with insulin allergy which manifested soon after COVID-19 vaccination. ...

    Abstract We experienced a case with insulin allergy which manifested soon after COVID-19 vaccination.
    MeSH term(s) Humans ; BNT162 Vaccine ; COVID-19 Vaccines ; COVID-19 ; Vaccination ; Insulins ; Hypersensitivity
    Chemical Substances BNT162 Vaccine ; COVID-19 Vaccines ; Insulins
    Language English
    Publishing date 2022-12-23
    Publishing country Japan
    Document type Letter
    ZDB-ID 2625840-7
    ISSN 2040-1124 ; 2040-1116
    ISSN (online) 2040-1124
    ISSN 2040-1116
    DOI 10.1111/jdi.13969
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  7. Article: [Regulation of Systemic Metabolism by Autonomic Nerve-Mediated Inter-Organ Networks].

    Imai, Junta / Katagiri, Hideki

    Brain and nerve = Shinkei kenkyu no shinpo

    2021  Volume 73, Issue 8, Page(s) 851–856

    Abstract: Autonomic nerves, including sympathetic nerves and parasympathetic nerves, innervate organs and modulate those function, thereby regulating systemic metabolism. Autonomic nerve bundles contain both afferent and efferent nerve fibers, and both fibers play ...

    Abstract Autonomic nerves, including sympathetic nerves and parasympathetic nerves, innervate organs and modulate those function, thereby regulating systemic metabolism. Autonomic nerve bundles contain both afferent and efferent nerve fibers, and both fibers play important roles in regulating systemic metabolism for maintenance of homeostasis at the whole-body level. Furthermore, recently-obtained evidence unraveled the metabolic regulatory systems through autonomic nerve-mediated inter-organ networks. In these systems, afferent innervations of autonomic nerves transmit metabolic information from peripheral organs to the central nervous system (CNS), and the CNS regulates organ functions based on the transmitted metabolic information through efferent innervations of autonomic nerves. In this review, autonomic nerve-mediated inter-organ networks that are involved in systemic metabolism are introduced, especially focusing on the liver-brain-pancreatic β-cell inter-organ network.
    MeSH term(s) Autonomic Nervous System ; Autonomic Pathways ; Central Nervous System ; Humans
    Language Japanese
    Publishing date 2021-08-10
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 390389-8
    ISSN 1344-8129 ; 1881-6096 ; 0006-8969
    ISSN (online) 1344-8129
    ISSN 1881-6096 ; 0006-8969
    DOI 10.11477/mf.1416201851
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    Zs.A 398: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  8. Article ; Online: Regulation of systemic metabolism by the autonomic nervous system consisting of afferent and efferent innervation.

    Imai, Junta / Katagiri, Hideki

    International immunology

    2021  Volume 34, Issue 2, Page(s) 67–79

    Abstract: Autonomic nerves, sympathetic and parasympathetic, innervate organs and modulate their functions. It has become evident that afferent and efferent signals of the autonomic nervous system play important roles in regulating systemic metabolism, thereby ... ...

    Abstract Autonomic nerves, sympathetic and parasympathetic, innervate organs and modulate their functions. It has become evident that afferent and efferent signals of the autonomic nervous system play important roles in regulating systemic metabolism, thereby maintaining homeostasis at the whole-body level. Vagal afferent nerves receive signals, such as nutrients and hormones, from the peripheral organs/tissues including the gastrointestinal tract and adipose tissue then transmit these signals to the hypothalamus, thereby regulating feeding behavior. In addition to roles in controlling appetite, areas in the hypothalamus serve as regulatory centers of both sympathetic and parasympathetic efferent fibers. These efferent innervations regulate the functions of peripheral organs/tissues, such as pancreatic islets, adipose tissues and the liver, which play roles in metabolic regulation. Furthermore, recent evidence has unraveled the metabolic regulatory systems governed by autonomic nerve circuits. In these systems, afferent nerves transmit metabolic information from peripheral organs to the central nervous system (CNS) and the CNS thereby regulates the organ functions through the efferent fibers of autonomic nerves. Thus, the autonomic nervous system regulates the homeostasis of systemic metabolism, and both afferent and efferent fibers play critical roles in its regulation. In addition, several lines of evidence demonstrate the roles of the autonomic nervous system in regulating and dysregulating the immune system. This review introduces variety of neuron-mediated inter-organ cross-talk systems and organizes the current knowledge of autonomic control/coordination of systemic metabolism, focusing especially on a liver-brain-pancreatic β-cell autonomic nerve circuit, as well as highlighting the potential importance of connections with the neuronal and immune systems.
    MeSH term(s) Autonomic Nervous System/metabolism ; Central Nervous System ; Islets of Langerhans ; Organogenesis ; Peripheral Nervous System
    Language English
    Publishing date 2021-04-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1013745-2
    ISSN 1460-2377 ; 0953-8178
    ISSN (online) 1460-2377
    ISSN 0953-8178
    DOI 10.1093/intimm/dxab023
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  9. Article ; Online: Type 1 Diabetes Mellitus Associated with Nivolumab after Second SARS-CoV-2 Vaccination, Japan.

    Sato, Toshihiro / Kodama, Shinjiro / Kaneko, Keizo / Imai, Junta / Katagiri, Hideki

    Emerging infectious diseases

    2022  Volume 28, Issue 7, Page(s) 1518–1520

    Abstract: Recently, along with increasing use of immune checkpoint inhibitors such as nivolumab, the incidence of immune-related adverse events, including type 1 diabetes mellitus, has become a serious problem. We report a patient who had immune checkpoint ... ...

    Abstract Recently, along with increasing use of immune checkpoint inhibitors such as nivolumab, the incidence of immune-related adverse events, including type 1 diabetes mellitus, has become a serious problem. We report a patient who had immune checkpoint inhibitor‒associated type 1 diabetes mellitus that developed after a second mRNA-based SARS-CoV-2 vaccination.
    MeSH term(s) COVID-19/prevention & control ; COVID-19 Vaccines/adverse effects ; Diabetes Mellitus, Type 1/chemically induced ; Humans ; Immune Checkpoint Inhibitors/adverse effects ; Japan ; Nivolumab/adverse effects ; SARS-CoV-2/immunology ; Vaccination/adverse effects
    Chemical Substances COVID-19 Vaccines ; Immune Checkpoint Inhibitors ; Nivolumab (31YO63LBSN)
    Language English
    Publishing date 2022-04-25
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 1380686-5
    ISSN 1080-6059 ; 1080-6040
    ISSN (online) 1080-6059
    ISSN 1080-6040
    DOI 10.3201/eid2807.220127
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    Zs.A 4778: Show issues Location:
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  10. Article: A Multicenter, Open-Label, Single-Arm Trial of the Efficacy and Safety of Empagliflozin Treatment for Refractory Diabetes Mellitus with Insulin Resistance (EMPIRE-01).

    Hirota, Yushi / Kakei, Yasumasa / Imai, Junta / Katagiri, Hideki / Ebihara, Ken / Wada, Jun / Suzuki, Junichi / Urakami, Tatsuhiko / Omori, Takashi / Ogawa, Wataru

    Diabetes therapy : research, treatment and education of diabetes and related disorders

    2024  Volume 15, Issue 2, Page(s) 533–545

    Abstract: Introduction: Insulin resistance syndrome and lipoatrophic diabetes are characterized by severe insulin resistance and are often refractory to treatment. Trials assessing the efficacy of antidiabetes drugs for these rare conditions have been limited, ... ...

    Abstract Introduction: Insulin resistance syndrome and lipoatrophic diabetes are characterized by severe insulin resistance and are often refractory to treatment. Trials assessing the efficacy of antidiabetes drugs for these rare conditions have been limited, however. Sodium-glucose cotransporter 2 (SGLT2) inhibitors, which lower glycemia independently of insulin action, have shown efficacy for type 2 diabetes with insulin resistance. We here investigated the efficacy and safety of the SGLT2 inhibitor empagliflozin for treatment of insulin resistance syndrome and lipoatrophic diabetes.
    Methods: The trial was conducted at five academic centers in Japan and included seven patients with insulin resistance syndrome and one patient with lipoatrophic diabetes. Participants received 10 mg of empagliflozin daily. If the hemoglobin A
    Results: By the end of the 24-week treatment period, the mean HbA
    Conclusion: Our results demonstrate that empagliflozin shows a certain level of efficacy and safety for treatment of insulin resistance syndrome and lipoatrophic diabetes.
    Trial registration: jRCTs2051190029 and NCT04018365.
    Language English
    Publishing date 2024-01-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2566702-6
    ISSN 1869-6961 ; 1869-6953
    ISSN (online) 1869-6961
    ISSN 1869-6953
    DOI 10.1007/s13300-023-01526-x
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