LIVIVO - Search results -

Search results

Result 1 - 10 of total 136

Search options

Article ; Online: Chloride transporters and channels in β-cell physiology: revisiting a 40-year-old model.

Di Fulvio, Mauricio / Aguilar-Bryan, Lydia

2020 Volume 47, Issue 6, Page(s) 1843–1855

Abstract: It is accepted that insulin-secreting β-cells release insulin in response to glucose even in the absence of functional ATP-sensitive K+ (KATP)-channels, which play a central role in a 'consensus model' of secretion broadly accepted and widely reproduced ... ...

Abstract	It is accepted that insulin-secreting β-cells release insulin in response to glucose even in the absence of functional ATP-sensitive K+ (KATP)-channels, which play a central role in a 'consensus model' of secretion broadly accepted and widely reproduced in textbooks. A major shortcoming of this consensus model is that it ignores any and all anionic mechanisms, known for more than 40 years, to modulate β-cell electrical activity and therefore insulin secretion. It is now clear that, in addition to metabolically regulated KATP-channels, β-cells are equipped with volume-regulated anion (Cl-) channels (VRAC) responsive to glucose concentrations in the range known to promote electrical activity and insulin secretion. In this context, the electrogenic efflux of Cl- through VRAC and other Cl- channels known to be expressed in β-cells results in depolarization because of an outwardly directed Cl- gradient established, maintained and regulated by the balance between Cl- transporters and channels. This review will provide a succinct historical perspective on the development of a complex hypothesis: Cl- transporters and channels modulate insulin secretion in response to nutrients.
MeSH term(s)	Animals ; Chlorides/metabolism ; Humans ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/physiology ; Ion Channels/metabolism ; Ion Transport ; Models, Biological
Chemical Substances	Chlorides ; Ion Channels
Language	English
Publishing date	2020-01-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20190513
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 944: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Correction: Heterogeneous expression of CFTR in insulin-secreting β-cells of the normal human islet.

Fulvio, Mauricio Di / Bogdani, Marika / Velasco, Myrian / McMillen, Timothy S / Ridaura, Cecilia / Kelly, Lisa / Almutairi, Mohammed M / Kursan, Shams / Sajib, Abu A / Hiriart, Marcia / Aguilar-Bryan, Lydia

PloS one

2023 Volume 18, Issue 7, Page(s) e0288417

Abstract: This corrects the article DOI: 10.1371/journal.pone.0242749.]. ...

Abstract	[This corrects the article DOI: 10.1371/journal.pone.0242749.].
Language	English
Publishing date	2023-07-07
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0288417
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Neonatal diabetes mellitus.

Aguilar-Bryan, Lydia / Bryan, Joseph

Endocrine reviews

2008 Volume 29, Issue 3, Page(s) 265–291

Abstract: An explosion of work over the last decade has produced insight into the multiple hereditary causes of a nonimmunological form of diabetes diagnosed most frequently within the first 6 months of life. These studies are providing increased understanding of ... ...

Abstract	An explosion of work over the last decade has produced insight into the multiple hereditary causes of a nonimmunological form of diabetes diagnosed most frequently within the first 6 months of life. These studies are providing increased understanding of genes involved in the entire chain of steps that control glucose homeostasis. Neonatal diabetes is now understood to arise from mutations in genes that play critical roles in the development of the pancreas, of beta-cell apoptosis and insulin processing, as well as the regulation of insulin release. For the basic researcher, this work is providing novel tools to explore fundamental molecular and cellular processes. For the clinician, these studies underscore the need to identify the genetic cause underlying each case. It is increasingly clear that the prognosis, therapeutic approach, and genetic counseling a physician provides must be tailored to a specific gene in order to provide the best medical care.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/physiopathology ; Diabetes Mellitus, Type 1/therapy ; Humans ; Hyperglycemia/genetics ; Hyperglycemia/physiopathology ; Hyperglycemia/therapy ; Infant, Newborn ; Infant, Newborn, Diseases/genetics ; Infant, Newborn, Diseases/physiopathology ; Infant, Newborn, Diseases/therapy
Language	English
Publishing date	2008-04-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/er.2007-0029
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1562: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Channel regulation of glucose sensing in the pancreatic beta-cell.

Hiriart, Marcia / Aguilar-Bryan, Lydia

American journal of physiology. Endocrinology and metabolism

2008 Volume 295, Issue 6, Page(s) E1298–306

Abstract: Mammalian beta-cells are acutely and chronically regulated by sensing surrounding glucose levels that determine the rate at which insulin is secreted, to maintain euglycemia. Experimental research in vitro and in vivo has shown that, when these cells are ...

Abstract	Mammalian beta-cells are acutely and chronically regulated by sensing surrounding glucose levels that determine the rate at which insulin is secreted, to maintain euglycemia. Experimental research in vitro and in vivo has shown that, when these cells are exposed to adverse conditions like long periods of hypoglycemia or hyperglycemia, their capability to sense glucose is decreased. Understanding the normal physiology and identifying the main players along this route becomes paramount. In this review, we have taken on the task of looking at the role that ion channels play in the regulation of this process, delineating the different families, and describing the signaling that parallels the glucose sensing process that results in insulin release.
MeSH term(s)	Animals ; Calcium Signaling/physiology ; Glucose/metabolism ; Glucose/pharmacology ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/physiology ; Membrane Potentials/physiology ; Models, Biological ; Potassium Channels/physiology ; Transient Receptor Potential Channels/physiology
Chemical Substances	Insulin ; Potassium Channels ; Transient Receptor Potential Channels ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2008-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.90493.2008
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Heterogeneous expression of CFTR in insulin-secreting β-cells of the normal human islet.

Di Fulvio, Mauricio / Bogdani, Marika / Velasco, Myrian / McMillen, Timothy S / Ridaura, Cecilia / Kelly, Lisa / Almutairi, Mohammed M / Kursan, Shams / Sajib, Abu A / Hiriart, Marcia / Aguilar-Bryan, Lydia

PloS one

2020 Volume 15, Issue 12, Page(s) e0242749

Abstract: Cystic fibrosis (CF) is due to mutations in the CF-transmembrane conductance regulator (CFTR) and CF-related diabetes (CFRD) is its most common co-morbidity, affecting ~50% of all CF patients, significantly influencing pulmonary function and longevity. ... ...

Abstract	Cystic fibrosis (CF) is due to mutations in the CF-transmembrane conductance regulator (CFTR) and CF-related diabetes (CFRD) is its most common co-morbidity, affecting ~50% of all CF patients, significantly influencing pulmonary function and longevity. Yet, the complex pathogenesis of CFRD remains unclear. Two non-mutually exclusive underlying mechanisms have been proposed in CFRD: i) damage of the endocrine cells secondary to the severe exocrine pancreatic pathology and ii) intrinsic β-cell impairment of the secretory response in combination with other factors. The later has proven difficult to determine due to low expression of CFTR in β-cells, which results in the general perception that this Cl-channel does not participate in the modulation of insulin secretion or the development of CFRD. The objective of the present work is to demonstrate CFTR expression at the molecular and functional levels in insulin-secreting β-cells in normal human islets, where it seems to play a role. Towards this end, we have used immunofluorescence confocal and immunofluorescence microscopy, immunohistochemistry, RT-qPCR, Western blotting, pharmacology, electrophysiology and insulin secretory studies in normal human, rat and mouse islets. Our results demonstrate heterogeneous CFTR expression in human, mouse and rat β-cells and provide evidence that pharmacological inhibition of CFTR influences basal and stimulated insulin secretion in normal mouse islets but not in islets lacking this channel, despite being detected by electrophysiological means in ~30% of β-cells. Therefore, our results demonstrate a potential role for CFTR in the pancreatic β-cell secretory response suggesting that intrinsic β-cell dysfunction may also participate in the pathogenesis of CFRD.
MeSH term(s)	Adult ; Aged ; Animals ; Antibodies/metabolism ; Antigens/metabolism ; Cell Line ; Cystic Fibrosis Transmembrane Conductance Regulator/immunology ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Female ; Humans ; Infant ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Male ; Mice ; Middle Aged ; Rats ; Reproducibility of Results ; Young Adult
Chemical Substances	Antibodies ; Antigens ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6)
Language	English
Publishing date	2020-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0242749
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Structural abnormalities in islets from very young children with cystic fibrosis may contribute to cystic fibrosis-related diabetes.

Bogdani, Marika / Blackman, Scott M / Ridaura, Cecilia / Bellocq, Jean-Pierre / Powers, Alvin C / Aguilar-Bryan, Lydia

Scientific reports

2017 Volume 7, Issue 1, Page(s) 17231

Abstract: Cystic fibrosis (CF)-related diabetes (CFRD) is thought to result from beta-cell injury due in part to pancreas exocrine damage and lipofibrosis. CFRD pancreata exhibit reduced islet density and altered cellular composition. To investigate a possible ... ...

Abstract	Cystic fibrosis (CF)-related diabetes (CFRD) is thought to result from beta-cell injury due in part to pancreas exocrine damage and lipofibrosis. CFRD pancreata exhibit reduced islet density and altered cellular composition. To investigate a possible etiology, we tested the hypothesis that such changes are present in CF pancreata before the development of lipofibrosis. We evaluated pancreas and islet morphology in tissues from very young CF children (<4 years of age), and adult patients with CF and CFRD. The relative number of beta-cells in young CF tissues was reduced by 50% or more when compared to age-matched controls. Furthermore, young CF tissues displayed significantly smaller insulin-positive areas, lower proportion of beta-cells positive for the proliferation marker Ki67 or the ductal marker CK19 vs. control subjects, and islet inflammatory cell infiltrates, independently of the severity of the exocrine lesion and in the absence of amyloid deposits. CFRD pancreata exhibited greater islet injury with further reduction in islet density, decreased relative beta-cell number, and presence of amyloid deposits. Together, these results strongly suggest that an early deficiency in beta-cell number in infants with CF may contribute to the development of glucose intolerance in the CF pediatric population, and to CFRD, later in life.
MeSH term(s)	Cell Proliferation ; Child, Preschool ; Cystic Fibrosis/metabolism ; Cystic Fibrosis/pathology ; Diabetes Complications/metabolism ; Diabetes Complications/pathology ; Female ; Glucose Tolerance Test ; Humans ; Insulin/metabolism ; Islets of Langerhans/metabolism ; Islets of Langerhans/pathology ; Male ; Pancreas, Exocrine/metabolism ; Pancreas, Exocrine/pathology
Chemical Substances	Insulin
Language	English
Publishing date	2017-12-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-17404-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Candida

Ortiz, Bryan / Aguilar, Kateryn / Galindo, Celeste / Molina, Lizzy / Fontecha, Gustavo

Current medical mycology

2023 Volume 8, Issue 3, Page(s) 1–8

Abstract: Background and purpose: Infections by emerging and multiresistant : Materials and methods: The prevalence of species within the : Results: A total of 11 species of : Conclusion: Reports on the distribution ... ...

Abstract	Background and purpose: Infections by emerging and multiresistant Materials and methods: The prevalence of species within the Results: A total of 11 species of Conclusion: Reports on the distribution of
Language	English
Publishing date	2023-03-27
Publishing country	Iran
Document type	Journal Article
ZDB-ID	3015705-5
ISSN	2423-3420 ; 2423-3439
ISSN (online)	2423-3420
ISSN	2423-3439
DOI	10.18502/cmm.8.3.11212
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Sodium channel beta1 regulatory subunit deficiency reduces pancreatic islet glucose-stimulated insulin and glucagon secretion.

Ernst, Sara J / Aguilar-Bryan, Lydia / Noebels, Jeffrey L

Endocrinology

2008 Volume 150, Issue 3, Page(s) 1132–1139

Abstract: Glucose-stimulated insulin and glucagon release regulates glucose homeostasis by an excitation-secretion coupling pathway beginning with ATP-sensitive K(+) channel closure, membrane depolarization, and entry of calcium ions to stimulate exocytosis. The ... ...

Abstract	Glucose-stimulated insulin and glucagon release regulates glucose homeostasis by an excitation-secretion coupling pathway beginning with ATP-sensitive K(+) channel closure, membrane depolarization, and entry of calcium ions to stimulate exocytosis. The contribution of voltage-gated sodium channels to this release pathway is still being elucidated. We demonstrate that loss of Scn1b, a major regulatory subunit expressed with Na(v)1.7 protein in mouse pancreatic islets, reduces glucose-stimulated insulin and glucagon secretion in vitro and in vivo, resulting in severe fed and fasting hypoglycemia. This genetic mouse model is the first to demonstrate that sodium channelopathy impairs the physiological excitation-release coupling pathway for pancreatic insulin and glucagon release.
MeSH term(s)	Animals ; Cells, Cultured ; Down-Regulation/drug effects ; Glucagon/metabolism ; Glucose/pharmacology ; Glucose Tolerance Test ; Hypoglycemia/genetics ; Hypoglycemia/metabolism ; Insulin/metabolism ; Insulin Secretion ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Sodium Channels/genetics ; Sodium Channels/metabolism ; Voltage-Gated Sodium Channel beta-1 Subunit
Chemical Substances	Insulin ; Scn1b protein, mouse ; Sodium Channels ; Voltage-Gated Sodium Channel beta-1 Subunit ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2008-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2008-0991
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.72: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Assembly, maturation, and turnover of K(ATP) channel subunits.

Crane, Ana / Aguilar-Bryan, Lydia

The Journal of biological chemistry

2003 Volume 279, Issue 10, Page(s) 9080–9090

Abstract: ATP-sensitive K(+), or K(ATP), channels are comprised of K(IR)6.x and sulfonylurea receptor (SUR) subunits that assemble as octamers, (K(IR)/SUR)(4). The assembly pathway is unknown. Pulse-labeling studies show that when K(IR)6.2 is expressed ... ...

Abstract	ATP-sensitive K(+), or K(ATP), channels are comprised of K(IR)6.x and sulfonylurea receptor (SUR) subunits that assemble as octamers, (K(IR)/SUR)(4). The assembly pathway is unknown. Pulse-labeling studies show that when K(IR)6.2 is expressed individually, its turnover is biphasic; approximately 60% is lost with t((1/2)) approximately 36 min. The remainder converts to a long-lived species (t((1/2)) approximately 26 h) with an estimated half-time of 1.2 h. Expressed alone, SUR1 has a long half-life, approximately 25.5 h. When K(IR)6.2 and SUR1 are co-expressed, they associate rapidly and the fast degradation of K(IR)6.2 is eliminated. Based on changes in the glycosylation state of SUR1, the half-time for the maturation of K(ATP) channels, including completion of assembly, transit to the Golgi, and glycosylation, is approximately 2.2 h. Estimation of the turnover rates of mature, fully glycosylated SUR1 associated with K(IR)6.2 and of K(IR)6.2 associated with Myc-tagged SUR1 gave similar values for the half-life of K(ATP) channels, a mean value of approximately 7.3 h. K(ATP) channel subunits in INS-1 beta-cells displayed qualitatively similar kinetics. The results imply the octameric channels are stable. Two mutations, K(IR)6.2 W91R and SUR1 DeltaF1388, identified in patients with the severe form of familial hyperinsulinism, profoundly alter the rate of K(IR)6.2 and SUR1 turnover, respectively. Both mutant subunits associate with their respective partners but dissociate freely and degrade rapidly. The data support models of channel formation in which K(IR)6.2-SUR1 heteromers assemble functional channels and are inconsistent with models where SUR1 can only assemble with K(IR)6.2 tetramers.
MeSH term(s)	Animals ; COS Cells ; Chlorocebus aethiops ; Cricetinae ; Humans ; Kinetics ; Mutation ; Potassium Channels, Inwardly Rectifying/chemistry ; Potassium Channels, Inwardly Rectifying/genetics ; Potassium Channels, Inwardly Rectifying/metabolism ; Protein Subunits/chemistry ; Protein Subunits/genetics ; Protein Subunits/metabolism
Chemical Substances	Potassium Channels, Inwardly Rectifying ; Protein Subunits
Language	English
Publishing date	2003-12-29
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M311079200
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.108: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Novel Nonimmunological Forms of {beta}-Cell Dysfunction: Diabetic Syndromes and Pathogenic Mechanisms.

Robertson, R Paul / Aguilar-Bryan, Lydia

Endocrine reviews

2008 Volume 29, Issue 3, Page(s) 253

MeSH term(s)	Diabetes Mellitus, Type 1/etiology ; Diabetes Mellitus, Type 1/physiopathology ; Humans ; Immune System/physiology ; Insulin-Secreting Cells/physiology
Language	English
Publishing date	2008-05
Publishing country	United States
Document type	Editorial ; Introductory Journal Article
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/er.2008-0012
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1562: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito