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Article ; Online: Mu opioid receptor: from pain to glucose metabolism.

Tudurí, Eva / Nogueiras, Ruben

2017 Volume 8, Issue 4, Page(s) 5643–5644

Language	English
Publishing date	2017-03-15
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.14231
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Insulinotropic Actions of GLP-1: How Much in the Brain and How Much in the Periphery?

Tudurí, Eva / Nogueiras, Ruben

Endocrinology

2017 Volume 158, Issue 7, Page(s) 2071–2073

MeSH term(s)	Animals ; Brain ; Gastric Inhibitory Polypeptide ; Glucagon-Like Peptide 1 ; Glucagon-Like Peptide-1 Receptor ; Glucose ; Homeostasis ; Male ; Nervous System ; Rats
Chemical Substances	Glucagon-Like Peptide-1 Receptor ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2017-09-07
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2017-00410
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Article ; Online: The pancreatic β-cell in ageing: Implications in age-related diabetes.

Tudurí, Eva / Soriano, Sergi / Almagro, Lucía / Montanya, Eduard / Alonso-Magdalena, Paloma / Nadal, Ángel / Quesada, Ivan

Ageing research reviews

2022 Volume 80, Page(s) 101674

Abstract: The prevalence of type 2 diabetes (T2D) and impaired glucose tolerance (IGT) increases with ageing. T2D generally results from progressive impairment of the pancreatic islets to adapt β-cell mass and function in the setting of insulin resistance and ... ...

Abstract	The prevalence of type 2 diabetes (T2D) and impaired glucose tolerance (IGT) increases with ageing. T2D generally results from progressive impairment of the pancreatic islets to adapt β-cell mass and function in the setting of insulin resistance and increased insulin demand. Several studies have shown an age-related decline in peripheral insulin sensitivity. However, a precise understanding of the pancreatic β-cell response in ageing is still lacking. In this review, we summarize the age-related alterations, adaptations and/or failures of β-cells at the molecular, morphological and functional levels in mouse and human. Age-associated alterations include processes such as β-cell proliferation, apoptosis and cell identity that can influence β-cell mass. Age-related changes also affect β-cell function at distinct steps including electrical activity, Ca
MeSH term(s)	Aging/metabolism ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin/metabolism ; Insulin Resistance ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Mice
Chemical Substances	Insulin
Language	English
Publishing date	2022-06-17
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2022.101674
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Article ; Online: The Effects of Aging on Male Mouse Pancreatic β-Cell Function Involve Multiple Events in the Regulation of Secretion: Influence of Insulin Sensitivity.

Tudurí, Eva / Soriano, Sergi / Almagro, Lucía / García-Heredia, Anabel / Rafacho, Alex / Alonso-Magdalena, Paloma / Nadal, Ángel / Quesada, Ivan

The journals of gerontology. Series A, Biological sciences and medical sciences

2021 Volume 77, Issue 3, Page(s) 405–415

Abstract: Aging is associated with a decline in peripheral insulin sensitivity and an increased risk of impaired glucose tolerance and type 2 diabetes. During conditions of reduced insulin sensitivity, pancreatic β cells undergo adaptive responses to increase ... ...

Abstract	Aging is associated with a decline in peripheral insulin sensitivity and an increased risk of impaired glucose tolerance and type 2 diabetes. During conditions of reduced insulin sensitivity, pancreatic β cells undergo adaptive responses to increase insulin secretion and maintain euglycemia. However, the existence and nature of β-cell adaptations and/or alterations during aging are still a matter of debate. In this study, we investigated the effects of aging on β-cell function from control (3-month-old) and aged (20-month-old) mice. Aged animals were further categorized into 2 groups: high insulin sensitive (aged-HIS) and low insulin sensitive (aged-LIS). Aged-LIS mice were hyperinsulinemic, glucose intolerant, and displayed impaired glucose-stimulated insulin and C-peptide secretion, whereas aged-HIS animals showed characteristics in glucose homeostasis similar to controls. In isolated β cells, we observed that glucose-induced inhibition of KATP channel activity was reduced with aging, particularly in the aged-LIS group. Glucose-induced islet NAD(P)H production was decreased in aged mice, suggesting impaired mitochondrial function. In contrast, voltage-gated Ca2+ currents were higher in aged-LIS β cells, and pancreatic islets of both aged groups displayed increased glucose-induced Ca2+ signaling and augmented insulin secretion compared with controls. Morphological analysis of pancreas sections also revealed augmented β-cell mass with aging, especially in the aged-LIS group, as well as ultrastructural β-cell changes. Altogether, these findings indicate that aged mouse β cells compensate for the aging-induced alterations in the stimulus-secretion coupling, particularly by adjusting their Ca2+ influx to ensure insulin secretion. These results also suggest that decreased peripheral insulin sensitivity exacerbates the effects of aging on β cells.
MeSH term(s)	Aging ; Animals ; Calcium ; Diabetes Mellitus, Type 2 ; Glucose ; Insulin/pharmacology ; Insulin Resistance ; Insulin-Secreting Cells ; Islets of Langerhans/physiology ; Male ; Mice
Chemical Substances	Insulin ; Glucose (IY9XDZ35W2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glab276
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Article ; Online: Morphological and functional adaptations of pancreatic alpha-cells during late pregnancy in the mouse.

Quesada-Candela, Cristina / Tudurí, Eva / Marroquí, Laura / Alonso-Magdalena, Paloma / Quesada, Ivan / Nadal, Ángel

Metabolism: clinical and experimental

2019 Volume 102, Page(s) 153963

Abstract: Background: Pregnancy represents a major metabolic challenge for the mother, and involves a compensatory response of the pancreatic beta-cell to maintain normoglycemia. However, although pancreatic alpha-cells play a key role in glucose homeostasis and ... ...

Abstract	Background: Pregnancy represents a major metabolic challenge for the mother, and involves a compensatory response of the pancreatic beta-cell to maintain normoglycemia. However, although pancreatic alpha-cells play a key role in glucose homeostasis and seem to be involved in gestational diabetes, there is no information about their potential adaptations or changes during pregnancy. Material and methods: Non-pregnant (controls) and pregnant C57BL/6 mice at gestational day 18.5 (G18.5) and their isolated pancreatic islets were used for in vivo and ex vivo studies, respectively. The effect of pregnancy hormones was tested in glucagon-secreting α-TC1.9 cells. Immunohistochemical analysis was performed in pancreatic slices. Glucagon gene expression was monitored by RT-qPCR. Glucagon secretion and plasma hormones were measured by ELISA. Results: Pregnant mice on G18.5 exhibited alpha-cell hypertrophy as well as augmented alpha-cell area and mass. This alpha-cell mass expansion was mainly due to increased proliferation. No changes in alpha-cell apoptosis, ductal neogenesis, or alpha-to-beta transdifferentiation were found compared with controls. Pregnant mice on G18.5 exhibited hypoglucagonemia. Additionally, in vitro glucagon secretion at low glucose levels was decreased in isolated islets from pregnant animals. Glucagon content was also reduced. Experiments in α-TC1.9 cells indicated that, unlike estradiol and progesterone, placental lactogens and prolactin stimulated alpha-cell proliferation. Placental lactogens, prolactin and estradiol also inhibited glucagon release from α-TC1.9 cells at low glucose levels. Conclusions: The pancreatic alpha-cell in mice undergoes several morphofunctional changes during late pregnancy, which may contribute to proper glucose homeostasis. Gestational hormones are likely involved in these processes.
MeSH term(s)	Adaptation, Physiological/physiology ; Animals ; Cell Count ; Cell Size ; Cells, Cultured ; Female ; Gestational Age ; Glucagon/metabolism ; Glucagon-Secreting Cells/cytology ; Glucagon-Secreting Cells/physiology ; Islets of Langerhans/cytology ; Islets of Langerhans/physiology ; Mice ; Mice, Inbred C57BL ; Placental Hormones/physiology ; Pregnancy
Chemical Substances	Placental Hormones ; Glucagon (9007-92-5)
Language	English
Publishing date	2019-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2019.153963
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Article ; Online: GPR55 and the regulation of glucose homeostasis.

Tudurí, Eva / López, Miguel / Diéguez, Carlos / Nadal, Angel / Nogueiras, Ruben

The international journal of biochemistry & cell biology

2017 Volume 88, Page(s) 204–207

Abstract: Pathophysiological conditions such as obesity and type 2 diabetes (T2D) are reportedly associated to over-activation of the endocannabinoid system (ECS). Therefore, modulation of the ECS offers potential therapeutic benefits on those diseases. GPR55, the ...

Abstract	Pathophysiological conditions such as obesity and type 2 diabetes (T2D) are reportedly associated to over-activation of the endocannabinoid system (ECS). Therefore, modulation of the ECS offers potential therapeutic benefits on those diseases. GPR55, the receptor for L-α-lysophosphatidylinositol (LPI) that has also affinity for various cannabinoid ligands, is distributed at the central and peripheral level and it is involved in several physiological processes. This review summarizes the localization and role of GPR55 in tissues that are crucial for the regulation of glucose metabolism, and provides an update on its contribution in obesity and insulin resistance. Finally, the therapeutic potential of targeting the GPR55 receptor is also discussed.
Language	English
Publishing date	2017-07
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2017.04.010
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Zs.A 431: Show issues

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Article: A Calcium-Dependent Chloride Current Increases Repetitive Firing in Mouse Sympathetic Neurons.

Martinez-Pinna, Juan / Soriano, Sergi / Tudurí, Eva / Nadal, Angel / de Castro, Fernando

Frontiers in physiology

2018 Volume 9, Page(s) 508

Abstract: ... ...

Abstract	Ca
Language	English
Publishing date	2018-05-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2018.00508
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Article ; Online: Glucagon-Like Peptide 1 Analogs and their Effects on Pancreatic Islets.

Tudurí, Eva / López, Miguel / Diéguez, Carlos / Nadal, Angel / Nogueiras, Rubén

Trends in endocrinology and metabolism: TEM

2016 Volume 27, Issue 5, Page(s) 304–318

Abstract: Glucagon-like peptide 1 (GLP-1) exerts many actions that improve glycemic control. GLP-1 stimulates glucose-stimulated insulin secretion and protects β cells, while its extrapancreatic effects include cardioprotection, reduction of hepatic glucose ... ...

Abstract	Glucagon-like peptide 1 (GLP-1) exerts many actions that improve glycemic control. GLP-1 stimulates glucose-stimulated insulin secretion and protects β cells, while its extrapancreatic effects include cardioprotection, reduction of hepatic glucose production, and regulation of satiety. Although an appealing antidiabetic drug candidate, the rapid degradation of GLP-1 by dipeptidyl peptidase 4 (DPP-4) means that its therapeutic use is unfeasible, and this prompted the development of two main GLP-1 therapies: long-acting GLP-1 analogs and DPP-4 inhibitors. In this review, we focus on the pancreatic effects exerted by current GLP-1 derivatives used to treat diabetes. Based on the results from in vitro and in vivo studies in humans and animal models, we describe the specific actions of GLP-1 analogs on the synthesis, processing, and secretion of insulin, islet morphology, and β cell proliferation and apoptosis.
Language	English
Publishing date	2016-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2016.03.004
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Article: GPR55 and the regulation of glucose homeostasis

Tudurí, Eva / Angel Nadal / Carlos Diéguez / Miguel López / Ruben Nogueiras

international journal of biochemistry & cell biology. 2017 July, v. 88

2017

Abstract	Pathophysiological conditions such as obesity and type 2 diabetes (T2D) are reportedly associated to over-activation of the endocannabinoid system (ECS). Therefore, modulation of the ECS offers potential therapeutic benefits on those diseases. GPR55, the receptor for L-α-lysophosphatidylinositol (LPI) that has also affinity for various cannabinoid ligands, is distributed at the central and peripheral level and it is involved in several physiological processes. This review summarizes the localization and role of GPR55 in tissues that are crucial for the regulation of glucose metabolism, and provides an update on its contribution in obesity and insulin resistance. Finally, the therapeutic potential of targeting the GPR55 receptor is also discussed.
Keywords	cannabinoids ; glucose ; homeostasis ; insulin resistance ; ligands ; metabolism ; noninsulin-dependent diabetes mellitus ; obesity ; tissues
Language	English
Dates of publication	2017-07
Size	p. 204-207.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2017.04.010
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Early overnutrition reduces Pdx1 expression and induces β cell failure in Swiss Webster mice.

Glavas, Maria M / Hui, Queenie / Tudurí, Eva / Erener, Suheda / Kasteel, Naomi L / Johnson, James D / Kieffer, Timothy J

Scientific reports

2019 Volume 9, Issue 1, Page(s) 3619

Abstract: Childhood obesity and early rapid growth increase the risk for type 2 diabetes. Such early overnutrition can be modeled in mice by reducing litter size. We investigated the effects of early overnutrition and increased dietary fat intake on β cell ... ...

Abstract	Childhood obesity and early rapid growth increase the risk for type 2 diabetes. Such early overnutrition can be modeled in mice by reducing litter size. We investigated the effects of early overnutrition and increased dietary fat intake on β cell function in Swiss Webster mice. On a moderate-fat diet, early overnutrition accelerated weight gain and induced hyperinsulinemia in pups. Early overnutrition males exhibited higher β cell mass but reduced islet insulin content and Pdx1 expression. Males had a high diabetes incidence that was increased by early overnutrition, characterized by a progressive increase in insulin secretion as well as β cell death, indicated by histological analysis and increased circulating miR-375 levels. Females maintained normoglycemia throughout life. High-fat diet (HFD) increased diabetes incidence in males, whereas low-fat diet was completely protective. This protective effect was abolished in early overnutrition males transiently exposed to HFD in early life. Although Swiss Webster mice are not known to be diabetes-prone, the high diabetes incidence suggests an underlying genetic susceptibility that can be induced by overnutrition and increased dietary fat intake in early life. Thus, the nutritional environment in early life may impact long-term β cell function and increase diabetes risk, particularly in genetically susceptible individuals.
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Body Weight ; Diabetes Mellitus, Experimental/etiology ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diet, High-Fat/adverse effects ; Female ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Insulin/metabolism ; Insulin Resistance ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Male ; Mice ; Overnutrition/complications ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Weight Gain
Chemical Substances	Blood Glucose ; Homeodomain Proteins ; Insulin ; Trans-Activators ; pancreatic and duodenal homeobox 1 protein
Language	English
Publishing date	2019-03-06
Publishing country	England
Document type	Journal Article ; 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/s41598-019-39177-3
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