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  1. Article ; Online: Can COVID-19 cause diabetes?

    Accili, Domenico

    Nature metabolism

    2021  Volume 3, Issue 2, Page(s) 123–125

    MeSH term(s) COVID-19/complications ; Diabetes Complications/epidemiology ; Diabetes Mellitus/etiology ; Humans ; Insulin-Secreting Cells/virology ; Ketosis/complications ; SARS-CoV-2
    Language English
    Publishing date 2021-01-12
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-020-00339-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Whither Type 1 Diabetes?

    Accili, Domenico

    The New England journal of medicine

    2020  Volume 383, Issue 21, Page(s) 2078–2079

    MeSH term(s) Adolescent ; Antibodies, Monoclonal ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Type 2 ; Humans
    Chemical Substances Antibodies, Monoclonal ; golimumab (91X1KLU43E)
    Language English
    Publishing date 2020-11-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMe2030472
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  3. Article ; Online: Reversing pancreatic β-cell dedifferentiation in the treatment of type 2 diabetes.

    Son, Jinsook / Accili, Domenico

    Experimental & molecular medicine

    2023  Volume 55, Issue 8, Page(s) 1652–1658

    Abstract: The maintenance of glucose homeostasis is fundamental for survival and health. Diabetes develops when glucose homeostasis fails. Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell failure. The failure of β-cells to ... ...

    Abstract The maintenance of glucose homeostasis is fundamental for survival and health. Diabetes develops when glucose homeostasis fails. Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell failure. The failure of β-cells to compensate for insulin resistance results in hyperglycemia, which in turn drives altered lipid metabolism and β-cell failure. Thus, insulin secretion by pancreatic β-cells is a primary component of glucose homeostasis. Impaired β-cell function and reduced β-cell mass are found in diabetes. Both features stem from a failure to maintain β-cell identity, which causes β-cells to dedifferentiate into nonfunctional endocrine progenitor-like cells or to trans-differentiate into other endocrine cell types. In this regard, one of the key issues in achieving disease modification is how to reestablish β-cell identity. In this review, we focus on the causes and implications of β-cell failure, as well as its potential reversibility as a T2D treatment.
    MeSH term(s) Humans ; Diabetes Mellitus, Type 2/metabolism ; Insulin/metabolism ; Cell Dedifferentiation ; Insulin Resistance ; Insulin-Secreting Cells/metabolism ; Glucose/metabolism
    Chemical Substances Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-08-01
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-023-01043-8
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    Zs.A 4775: Show issues Location:
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  4. Article ; Online: Unraveling the mysteries of hepatic insulin signaling: deconvoluting the nuclear targets of insulin.

    Kitamoto, Takumi / Accili, Domenico

    Endocrine journal

    2023  Volume 70, Issue 9, Page(s) 851–866

    Abstract: Over 100 years have passed since insulin was first administered to a diabetic patient. Since then great strides have been made in diabetes research. It has determined where insulin is secreted from, which organs it acts on, how it is transferred into the ...

    Abstract Over 100 years have passed since insulin was first administered to a diabetic patient. Since then great strides have been made in diabetes research. It has determined where insulin is secreted from, which organs it acts on, how it is transferred into the cell and is delivered to the nucleus, how it orchestrates the expression pattern of the genes, and how it works with each organ to maintain systemic metabolism. Any breakdown in this system leads to diabetes. Thanks to the numerous researchers who have dedicated their lives to cure diabetes, we now know that there are three major organs where insulin acts to maintain glucose/lipid metabolism: the liver, muscles, and fat. The failure of insulin action on these organs, such as insulin resistance, result in hyperglycemia and/or dyslipidemia. The primary trigger of this condition and its association among these tissues still remain to be uncovered. Among the major organs, the liver finely tunes the glucose/lipid metabolism to maintain metabolic flexibility, and plays a crucial role in glucose/lipid abnormality due to insulin resistance. Insulin resistance disrupts this tuning, and selective insulin resistance arises. The glucose metabolism loses its sensitivity to insulin, while the lipid metabolism maintains it. The clarification of its mechanism is warranted to reverse the metabolic abnormalities due to insulin resistance. This review will provide a brief historical review for the progress of the pathophysiology of diabetes since the discovery of insulin, followed by a review of the current research clarifying our understanding of selective insulin resistance.
    MeSH term(s) Humans ; Insulin/metabolism ; Insulin Resistance/physiology ; Liver/metabolism ; Diabetes Mellitus/metabolism ; Glucose/metabolism ; Lipid Metabolism ; Diabetes Mellitus, Type 2/metabolism
    Chemical Substances Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-05-27
    Publishing country Japan
    Document type Review ; Journal Article
    ZDB-ID 1151918-6
    ISSN 1348-4540 ; 0918-8959
    ISSN (online) 1348-4540
    ISSN 0918-8959
    DOI 10.1507/endocrj.EJ23-0150
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  5. Article ; Online: Insulin Action Research and the Future of Diabetes Treatment: The 2017 Banting Medal for Scientific Achievement Lecture.

    Accili, Domenico

    Diabetes

    2018  Volume 67, Issue 9, Page(s) 1701–1709

    Abstract: Diabetes is caused by combined abnormalities in insulin production and action. The pathophysiology of these defects has been studied extensively and is reasonably well understood. Their causes are elusive and their manifestations pleiotropic, likely ... ...

    Abstract Diabetes is caused by combined abnormalities in insulin production and action. The pathophysiology of these defects has been studied extensively and is reasonably well understood. Their causes are elusive and their manifestations pleiotropic, likely reflecting the triple threat of genes, environment, and lifestyle. Treatment, once restricted to monotherapy with secretagogues or insulin, now involves complex combinations of expensive regimens that stem the progression but do not fundamentally alter the underlying causes of the disease. As advances in our understanding of insulin action and β-cell failure reach a critical stage, here I draw on lessons learned from our research on insulin regulation of gene expression and pancreatic β-cell dedifferentiation to address the question of how we can translate this exciting biology into mechanism-based interventions to reverse the course of diabetes.
    MeSH term(s) Animals ; Awards and Prizes ; Cell Dedifferentiation/drug effects ; Cell Transdifferentiation/drug effects ; Cellular Reprogramming/drug effects ; Combined Modality Therapy/adverse effects ; Diabetes Complications/prevention & control ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/drug therapy ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/therapy ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/therapy ; Drug Design ; Drug Therapy, Combination/adverse effects ; Enteroendocrine Cells/drug effects ; Enteroendocrine Cells/metabolism ; Enteroendocrine Cells/pathology ; Forkhead Transcription Factors/antagonists & inhibitors ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Humans ; Hypoglycemic Agents/adverse effects ; Hypoglycemic Agents/chemistry ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Insulin/adverse effects ; Insulin/metabolism ; Insulin/pharmacology ; Insulin/therapeutic use ; Insulin Resistance ; Insulin Secretion ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Models, Biological
    Chemical Substances Forkhead Transcription Factors ; Hypoglycemic Agents ; Insulin
    Language English
    Publishing date 2018-08-22
    Publishing country United States
    Document type Journal Article ; Lecture ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi18-0025
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  6. Book: Genetic manipulation of receptor expression and function

    Accili, Domenico

    (Receptor biochemistry and methodology)

    2000  

    Author's details ed. by Domenico Accili
    Series title Receptor biochemistry and methodology
    Keywords Rezeptor ; Gen-Targeting ; Genexpression
    Language English
    Size XII, 240 S. : Ill., graph. Darst.
    Publisher Wiley-Liss
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT012740902
    ISBN 0-471-35057-5 ; 978-0-471-35057-6
    Database Catalogue ZB MED Medicine, Health

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    2000 A 2047 order for loan Magazin

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  7. Book: Mechanisms of insulin action

    Accili, Domenico / Saltiel, Alan R.

    (Medical intelligence unit)

    2007  

    Author's details Alan R. Saltiel ... [ed. Contrib. Domenico Accili
    Series title Medical intelligence unit
    Keywords Insulin / pharmacology
    Language English
    Size XI, 214 S. : Ill., graph. Darst., 248 mm x 165 mm
    Publisher Landes Bioscience ; Springer Science+Business Media
    Publishing place Austin, Tex ; New York, NY
    Publishing country United States
    Document type Book
    HBZ-ID HT015306894
    ISBN 978-0-387-72203-0 ; 0-387-72203-3
    Database Catalogue ZB MED Medicine, Health

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  8. Article ; Online: Ceci n'est pas science.

    Accili, Domenico

    Cell metabolism

    2015  Volume 21, Issue 4, Page(s) 503–504

    Abstract: Biomedical research is not immune to economic imperatives. But as the realities of profit encroach ever closer on what was once regarded as an idealistic and selfless endeavor, the author reflects on four trends that are hollowing out the research ... ...

    Abstract Biomedical research is not immune to economic imperatives. But as the realities of profit encroach ever closer on what was once regarded as an idealistic and selfless endeavor, the author reflects on four trends that are hollowing out the research enterprise.
    MeSH term(s) Academic Medical Centers/economics ; Academic Medical Centers/trends ; Biomedical Research/economics ; Biomedical Research/standards ; Capitalism ; Drug Industry/methods ; Drug Industry/standards ; Fund Raising/methods ; Fund Raising/standards ; Humans
    Language English
    Publishing date 2015-04-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2015.03.011
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    Zs.A 6169: Show issues Location:
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  9. Article ; Online: Cyb5r3 activation rescues secondary failure to sulfonylurea but not β-cell dedifferentiation.

    Watanabe, Hitoshi / Asahara, Shun-Ichiro / Son, Jinsook / McKimpson, Wendy M / de Cabo, Rafael / Accili, Domenico

    PloS one

    2024  Volume 19, Issue 2, Page(s) e0297555

    Abstract: Diabetes mellitus is characterized by insulin resistance and β-cell failure. The latter involves impaired insulin secretion and β-cell dedifferentiation. Sulfonylurea (SU) is used to improve insulin secretion in diabetes, but it suffers from secondary ... ...

    Abstract Diabetes mellitus is characterized by insulin resistance and β-cell failure. The latter involves impaired insulin secretion and β-cell dedifferentiation. Sulfonylurea (SU) is used to improve insulin secretion in diabetes, but it suffers from secondary failure. The relationship between SU secondary failure and β-cell dedifferentiation has not been examined. Using a model of SU secondary failure, we have previously shown that functional loss of oxidoreductase Cyb5r3 mediates effects of SU failure through interactions with glucokinase. Here we demonstrate that SU failure is associated with partial β-cell dedifferentiation. Cyb5r3 knockout mice show more pronounced β-cell dedifferentiation and glucose intolerance after chronic SU administration, high-fat diet feeding, and during aging. A Cyb5r3 activator improves impaired insulin secretion caused by chronic SU treatment, but not β-cell dedifferentiation. We conclude that chronic SU administration affects progression of β-cell dedifferentiation and that Cyb5r3 activation reverses secondary failure to SU without restoring β-cell dedifferentiation.
    MeSH term(s) Animals ; Mice ; Cell Dedifferentiation ; Diabetes Mellitus, Type 2/drug therapy ; Insulin/pharmacology ; Insulin Resistance ; Insulin-Secreting Cells ; Sulfonylurea Compounds/pharmacology ; Cytochrome-B(5) Reductase/genetics ; Cytochrome-B(5) Reductase/metabolism
    Chemical Substances Insulin ; Sulfonylurea Compounds ; Cyb5r3 protein, mouse (EC 1.6.2.2) ; Cytochrome-B(5) Reductase (EC 1.6.2.2)
    Language English
    Publishing date 2024-02-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0297555
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  10. Article ; Online: β-cell Jagged1 is sufficient but not necessary for islet Notch activity and insulin secretory defects in obese mice.

    Suda, Nina / Bartolomé, Alberto / Liang, Jiani / Son, Jinsook / Yagishita, Yoko / Siebel, Christian / Accili, Domenico / Ding, Hongxu / Pajvani, Utpal B

    Molecular metabolism

    2024  Volume 81, Page(s) 101894

    Abstract: Objective: Notch signaling, re-activated in β cells from obese mice and causal to β cell dysfunction, is determined in part by transmembrane ligand availability in a neighboring cell. We hypothesized that β cell expression of Jagged1 determines the ... ...

    Abstract Objective: Notch signaling, re-activated in β cells from obese mice and causal to β cell dysfunction, is determined in part by transmembrane ligand availability in a neighboring cell. We hypothesized that β cell expression of Jagged1 determines the maladaptive Notch response and resultant insulin secretory defects in obese mice.
    Methods: We assessed expression of Notch pathway components in high-fat diet-fed (HFD) or leptin receptor-deficient (db/db) mice, and performed single-cell RNA sequencing (scRNA-Seq) in islets from patients with and without type 2 diabetes (T2D). We generated and performed glucose tolerance testing in inducible, β cell-specific Jagged1 gain-of- and loss-of-function mice. We also tested effects of monoclonal neutralizing antibodies to Jagged1 in glucose-stimulated insulin secretion (GSIS) assays in isolated islets.
    Results: Jag1 was the only Notch ligand that tracked with increased Notch activity in HFD-fed and db/db mice, as well as in metabolically-inflexible β cells enriched in patients with T2D. Neutralizing antibodies to block Jagged1 in islets isolated from HFD-fed and db/db mice potentiated GSIS ex vivo. To demonstrate if β cell Jagged1 is sufficient to cause glucose tolerance in vivo, we generated inducible β cell-specific Jag1 transgenic (β-Jag1
    Conclusions: Jagged1 is increased in islets from obese mice and in patients with T2D, and neutralizing Jagged1 antibodies lead to improved GSIS, suggesting that inhibition of Jagged1-Notch signaling may have therapeutic benefit. However, genetic loss-of-function experiments suggest that β cells are not a likely source of the Jagged1 signal.
    MeSH term(s) Animals ; Humans ; Mice ; Antibodies, Neutralizing ; Diabetes Mellitus, Type 2/genetics ; Glucose/metabolism ; Insulin/metabolism ; Ligands ; Mice, Obese
    Chemical Substances Antibodies, Neutralizing ; Glucose (IY9XDZ35W2) ; Insulin ; Ligands ; Jag1 protein, mouse
    Language English
    Publishing date 2024-02-03
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2024.101894
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