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Article ; Online: The Pancreatic Beta Cell: Editorial.

Bartolomé, Alberto

2023 Volume 13, Issue 3

Abstract: Pancreatic beta cells play a critical role in maintaining glucose homeostasis by serving as the primary source of insulin [ ... ]. ...

Abstract	Pancreatic beta cells play a critical role in maintaining glucose homeostasis by serving as the primary source of insulin [...].
MeSH term(s)	Insulin-Secreting Cells/metabolism ; Glucose/metabolism ; Insulin/metabolism ; Insulin Secretion
Chemical Substances	Glucose (IY9XDZ35W2) ; Insulin
Language	English
Publishing date	2023-03-08
Publishing country	Switzerland
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13030495
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Stem Cell-Derived β Cells: A Versatile Research Platform to Interrogate the Genetic Basis of β Cell Dysfunction.

Bartolomé, Alberto

International journal of molecular sciences

2022 Volume 23, Issue 1

Abstract: Pancreatic β cell dysfunction is a central component of diabetes progression. During the last decades, the genetic basis of several monogenic forms of diabetes has been recognized. Genome-wide association studies (GWAS) have also facilitated the ... ...

Abstract	Pancreatic β cell dysfunction is a central component of diabetes progression. During the last decades, the genetic basis of several monogenic forms of diabetes has been recognized. Genome-wide association studies (GWAS) have also facilitated the identification of common genetic variants associated with an increased risk of diabetes. These studies highlight the importance of impaired β cell function in all forms of diabetes. However, how most of these risk variants confer disease risk, remains unanswered. Understanding the specific contribution of genetic variants and the precise role of their molecular effectors is the next step toward developing treatments that target β cell dysfunction in the era of personalized medicine. Protocols that allow derivation of β cells from pluripotent stem cells, represent a powerful research tool that allows modeling of human development and versatile experimental designs that can be used to shed some light on diabetes pathophysiology. This article reviews different models to study the genetic basis of β cell dysfunction, focusing on the recent advances made possible by stem cell applications in the field of diabetes research.
MeSH term(s)	Animals ; Diabetes Mellitus/etiology ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/physiopathology ; Genome-Wide Association Study ; Humans ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/physiology ; Models, Biological ; Pluripotent Stem Cells ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2022-01-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23010501
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Article ; Online: MTOR and Beta Cell Adaptation in T2D.

Bartolomé, Alberto / Pajvani, Utpal B

The Journal of clinical endocrinology and metabolism

2020 Volume 106, Issue 3, Page(s) e1466–e1467

MeSH term(s)	Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-12-03
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgaa906
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Article ; Online: MafA Regulation in β-Cells: From Transcriptional to Post-Translational Mechanisms.

Liang, Jiani / Chirikjian, Margot / Pajvani, Utpal B / Bartolomé, Alberto

Biomolecules

2022 Volume 12, Issue 4

Abstract: β-cells are insulin-producing cells in the pancreas that maintain euglycemic conditions. Pancreatic β-cell maturity and function are regulated by a variety of transcription factors that enable the adequate expression of the cellular machinery involved in ...

Abstract	β-cells are insulin-producing cells in the pancreas that maintain euglycemic conditions. Pancreatic β-cell maturity and function are regulated by a variety of transcription factors that enable the adequate expression of the cellular machinery involved in nutrient sensing and commensurate insulin secretion. One of the key factors in this regulation is MAF bZIP transcription factor A (MafA). MafA expression is decreased in type 2 diabetes, contributing to β-cell dysfunction and disease progression. The molecular biology underlying MafA is complex, with numerous transcriptional and post-translational regulatory nodes. Understanding these complexities may uncover potential therapeutic targets to ameliorate β-cell dysfunction. This article will summarize the role of MafA in normal β-cell function and disease, with a special focus on known transcriptional and post-translational regulators of MafA expression.
MeSH term(s)	Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Maf Transcription Factors, Large/genetics ; Maf Transcription Factors, Large/metabolism
Chemical Substances	Insulin ; Maf Transcription Factors, Large
Language	English
Publishing date	2022-03-31
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12040535
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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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: An Overfeeding-Induced Obesity Mouse Model Reveals Necessity for Sin3a in Postnatal Peak β-Cell Mass Acquisition.

Bartolomé, Alberto / Ravussin, Yann / Yu, Junjie / Ferrante, Anthony W / Pajvani, Utpal B

Diabetes

2022 Volume 71, Issue 11, Page(s) 2395–2401

Abstract: The increase of functional β-cell mass is paramount to maintaining glucose homeostasis in the setting of systemic insulin resistance and/or augmented metabolic load. Understanding compensatory mechanisms that allow β-cell mass adaptation may allow for ... ...

Abstract	The increase of functional β-cell mass is paramount to maintaining glucose homeostasis in the setting of systemic insulin resistance and/or augmented metabolic load. Understanding compensatory mechanisms that allow β-cell mass adaptation may allow for the discovery of therapeutically actionable control nodes. In this study, we report the rapid and robust β-cell hyperplasic effect in a mouse model of overfeeding-induced obesity (OIO) based on direct gastric caloric infusion. By performing RNA sequencing in islets isolated from OIO mice, we identified Sin3a as a novel transcriptional regulator of β-cell mass adaptation. β-Cell-specific Sin3a knockout animals showed profound diabetes due to defective acquisition of postnatal β-cell mass. These findings reveal a novel regulatory pathway in β-cell proliferation and validate OIO as a model for discovery of other mechanistic determinants of β-cell adaptation.
MeSH term(s)	Mice ; Animals ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Obesity/genetics ; Obesity/metabolism ; Insulin Resistance ; Disease Models, Animal ; Glucose/metabolism
Chemical Substances	Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-08-09
Publishing country	United States
Document type	Journal Article ; 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/db22-0306
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Article ; Online: Angiotensin converting enzyme 2 is a novel target of the γ-secretase complex.

Bartolomé, Alberto / Liang, Jiani / Wang, Pengfei / Ho, David D / Pajvani, Utpal B

Scientific reports

2021 Volume 11, Issue 1, Page(s) 9803

Abstract: Angiotensin converting enzyme 2 (ACE2) is a key regulator of the renin-angiotensin system, but also the functional receptor of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Based on structural similarity with other γ-secretase (γS) ... ...

Abstract	Angiotensin converting enzyme 2 (ACE2) is a key regulator of the renin-angiotensin system, but also the functional receptor of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Based on structural similarity with other γ-secretase (γS) targets, we hypothesized that ACE2 may be affected by γS proteolytic activity. We found that after ectodomain shedding, ACE2 is targeted for intramembrane proteolysis by γS, releasing a soluble ACE2 C-terminal fragment. Consistently, chemical or genetic inhibition of γS results in the accumulation of a membrane-bound fragment of ectodomain-deficient ACE2. Although chemical inhibition of γS does not alter SARS-CoV-2 cell entry, these data point to a novel pathway for cellular ACE2 trafficking.
MeSH term(s)	Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; Animals ; COVID-19/genetics ; COVID-19/metabolism ; Caco-2 Cells ; Cell Line ; Chlorocebus aethiops ; Gene Knockout Techniques ; HEK293 Cells ; Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Presenilin-1/genetics ; Presenilin-1/metabolism ; Presenilin-2/genetics ; Presenilin-2/metabolism ; Proteolysis ; SARS-CoV-2/physiology ; Vero Cells ; Virus Internalization
Chemical Substances	Membrane Glycoproteins ; Presenilin-1 ; Presenilin-2 ; nicastrin protein ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2021-05-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-89379-x
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Article ; Online: Notch-mediated Ephrin signaling disrupts islet architecture and β cell function.

Bartolomé, Alberto / Suda, Nina / Yu, Junjie / Zhu, Changyu / Son, Jinsook / Ding, Hongxu / Califano, Andrea / Accili, Domenico / Pajvani, Utpal B

JCI insight

2022 Volume 7, Issue 6

Abstract: Altered islet architecture is associated with β cell dysfunction and type 2 diabetes (T2D) progression, but molecular effectors of islet spatial organization remain mostly unknown. Although Notch signaling is known to regulate pancreatic development, we ... ...

Abstract	Altered islet architecture is associated with β cell dysfunction and type 2 diabetes (T2D) progression, but molecular effectors of islet spatial organization remain mostly unknown. Although Notch signaling is known to regulate pancreatic development, we observed "reactivated" β cell Notch activity in obese mouse models. To test the repercussions and reversibility of Notch effects, we generated doxycycline-dependent, β cell-specific Notch gain-of-function mice. As predicted, we found that Notch activation in postnatal β cells impaired glucose-stimulated insulin secretion and glucose intolerance, but we observed a surprising remnant glucose intolerance after doxycycline withdrawal and cessation of Notch activity, associated with a marked disruption of normal islet architecture. Transcriptomic screening of Notch-active islets revealed increased Ephrin signaling. Commensurately, exposure to Ephrin ligands increased β cell repulsion and impaired murine and human pseudoislet formation. Consistent with our mouse data, Notch and Ephrin signaling were increased in metabolically inflexible β cells in patients with T2D. These studies suggest that β cell Notch/Ephrin signaling can permanently alter islet architecture during a morphogenetic window in early life.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 2/metabolism ; Doxycycline/metabolism ; Ephrins/metabolism ; Glucose Intolerance/metabolism ; Humans ; Insulin-Secreting Cells ; Islets of Langerhans/metabolism ; Mice
Chemical Substances	Ephrins ; Doxycycline (N12000U13O)
Language	English
Publishing date	2022-03-22
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.157694
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Article: How has COVID-19 modified training and mood in professional and non-professional football players?

Mon-López, Daniel / García-Aliaga, Abraham / Ginés Bartolomé, Alberto / Muriarte Solana, Diego

Physiology & behavior. 2020 Dec. 01, v. 227

2020

Abstract: Coronavirus disease 2019 (COVID-19) has restricted freedom of movement with several countries ‘locked down’ worldwide. During this isolation period or quarantine, habits have been modified. This might have had negative effects on physiological variables ... ...

Abstract	Coronavirus disease 2019 (COVID-19) has restricted freedom of movement with several countries ‘locked down’ worldwide. During this isolation period or quarantine, habits have been modified. This might have had negative effects on physiological variables but also influenced numerous emotional aspects, especially in elite athletes, which can have a negative impact on training and sleep quality, affecting their performance.175 Spanish professional and non-professional association football players answered an online survey about demographic and training habits, as well as two validated questionnaires to assess psychological variables (POMS and WLEIS-S).The results showed that the confinement period reduced the load of training (p < 0.01), and modified the sleeping behaviour (both, sleep time (p < 0.05) and quality (p < 0.001)) across soccer players. Higher emotional intelligence (EI) values were positively related to training variables and strongly correlated with the mood. Interestingly, athletes’ mood was affected differently depending on gender.We found that confinement period affects both, training load and recovery process and that mood states and EI could predict the training variables and performance of top-level football players.
Keywords	COVID-19 infection ; behavior ; emotions ; quarantine ; sleep ; sports ; surveys
Language	English
Dates of publication	2020-1201
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-light
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2020.113148
Database	NAL-Catalogue (AGRICOLA)

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Article: Angiotensin converting enzyme 2 is a novel target of the γ-secretase complex.

Bartolomé, Alberto / Liang, Jiani / Wang, Pengfei / Ho, David D / Pajvani, Utpal B

bioRxiv : the preprint server for biology

2020

Abstract	Angiotensin converting enzyme 2 (ACE2) is a key regulator of the renin-angiotensin system, but also the functional receptor of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Based on structural similarity with other γ-secretase (γS) targets, we hypothesized that ACE2 may be affected by γS proteolytic activity. We found that after ectodomain shedding, ACE2 is targeted for intramembrane proteolysis by γS, releasing a soluble ACE2 C-terminal fragment. Consistently, chemical or genetic inhibition of γS results in the accumulation of a membrane-bound fragment of ectodomain-deficient ACE2. Although chemical inhibition of γS does not alter SARS-CoV-2 cell entry, these data point to a novel pathway for cellular ACE2 trafficking.
Keywords	covid19
Language	English
Publishing date	2020-09-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.09.01.277954
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