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Article: Editorial: Mitochondrial Proteomics: Understanding Mitochondria Function and Dysfunction Through the Characterization of Their Proteome.

Ferri, Alberto / Garcia-Roves, Pablo M / Pieroni, Luisa

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 608753

Language	English
Publishing date	2020-12-10
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.608753
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Article: Impact of GLP-1 receptor agonist versus omega-3 fatty acids supplement on obesity-induced alterations of mitochondrial respiration.

Jansen, Kirsten M / Dahdah, Norma / Gama-Perez, Pau / Schots, Pauke C / Larsen, Terje S / Garcia-Roves, Pablo M

Frontiers in endocrinology

2023 Volume 14, Page(s) 1098391

Abstract: Objective: To compare administration of the glucagon-like peptide-1 (GLP-1) analogue, exenatide, versus dietary supplementation with the omega-3 fatty acid-rich Calanus oil on obesity-induced alterations in mitochondrial respiration.: Methods: Six- ... ...

Abstract	Objective: To compare administration of the glucagon-like peptide-1 (GLP-1) analogue, exenatide, versus dietary supplementation with the omega-3 fatty acid-rich Calanus oil on obesity-induced alterations in mitochondrial respiration. Methods: Six-week-old female C57BL/6JOlaHSD mice were given high fat diet (HFD, 45% energy from fat) for 12 weeks to induce obesity. Thereafter, they were divided in three groups where one received exenatide (10 μg/kg/day) via subcutaneously implanted mini-osmotic pumps, a second group received 2% Calanus oil as dietary supplement, while the third group received HFD without any treatment. Animals were sacrificed after 8 weeks of treatment and tissues (skeletal muscle, liver, and white adipose tissue) were collected for measurement of mitochondrial respiratory activity by high-resolution respirometry, using an Oroboros Oxygraph-2k (Oroboros instruments, Innsbruck, Austria). Results: It was found that high-fat feeding led to a marked reduction of mitochondrial respiration in adipose tissue during all three states investigated - LEAK, OXPHOS and ETS. This response was to some extent attenuated by exenatide treatment, but not with Calanus oil treatment. High-fat feeding had no major effect on hepatic mitochondrial respiration, but exenatide treatment resulted in a significant increase in the various respiratory states in liver. Mitochondrial respiration in skeletal muscle was not significantly influenced by high-fat diet or any of the treatments. The precise evaluation of mitochondrial respiration considering absolute oxygen flux and ratios to assess flux control efficiency avoided misinterpretation of the results. Conclusions: Exenatide increased hepatic mitochondrial respiration in high-fat fed mice, but no clear beneficial effect was observed in skeletal muscle or fat tissue. Calanus oil did not negatively affect respiratory activity in these tissues, which maintains its potential as a dietary supplement, due to its previously reported benefits on cardiac function.
MeSH term(s)	Mice ; Animals ; Female ; Exenatide ; Glucagon-Like Peptide-1 Receptor ; Mice, Inbred C57BL ; Obesity/drug therapy ; Obesity/etiology ; Fatty Acids, Omega-3/pharmacology ; Dietary Supplements ; Respiration
Chemical Substances	Exenatide (9P1872D4OL) ; Glucagon-Like Peptide-1 Receptor ; Fatty Acids, Omega-3
Language	English
Publishing date	2023-03-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1098391
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Article ; Online: Glycosylation defects, offset by PEPCK-M, drive entosis in breast carcinoma cells.

Hyroššová, Petra / Aragó, Marc / Muñoz-Pinedo, Cristina / Viñals, Francesc / García-Rovés, Pablo M / Escolano, Carmen / Méndez-Lucas, Andrés / Perales, Jose C

Cell death & disease

2022 Volume 13, Issue 8, Page(s) 730

Abstract: On glucose restriction, epithelial cells can undergo entosis, a cell-in-cell cannibalistic process, to allow considerable withstanding to this metabolic stress. Thus, we hypothesized that reduced protein glycosylation might participate in the activation ... ...

Abstract	On glucose restriction, epithelial cells can undergo entosis, a cell-in-cell cannibalistic process, to allow considerable withstanding to this metabolic stress. Thus, we hypothesized that reduced protein glycosylation might participate in the activation of this cell survival pathway. Glucose deprivation promoted entosis in an MCF7 breast carcinoma model, as evaluated by direct inspection under the microscope, or revealed by a shift to apoptosis + necrosis in cells undergoing entosis treated with a Rho-GTPase kinase inhibitor (ROCKi). In this context, curbing protein glycosylation defects with N-acetyl-glucosamine partially rescued entosis, whereas limiting glycosylation in the presence of glucose with tunicamycin or NGI-1, but not with other unrelated ER-stress inducers such as thapsigargin or amino-acid limitation, stimulated entosis. Mitochondrial phosphoenolpyruvate carboxykinase (PEPCK-M; PCK2) is upregulated by glucose deprivation, thereby enhancing cell survival. Therefore, we presumed that PEPCK-M could play a role in this process by offsetting key metabolites into glycosyl moieties using alternative substrates. PEPCK-M inhibition using iPEPCK-2 promoted entosis in the absence of glucose, whereas its overexpression inhibited entosis. PEPCK-M inhibition had a direct role on total protein glycosylation as determined by Concanavalin A binding, and the specific ratio of fully glycosylated LAMP1 or E-cadherin. The content of metabolites, and the fluxes from
MeSH term(s)	Breast Neoplasms ; Entosis ; Female ; Glucose/metabolism ; Glycosylation ; Humans ; Phosphoenolpyruvate Carboxykinase (ATP)/metabolism
Chemical Substances	PCK2 protein, human (EC 4.1.1.49) ; Phosphoenolpyruvate Carboxykinase (ATP) (EC 4.1.1.49) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-08-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-022-05177-x
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Article ; Online: Mitochondrial pathophysiology and type 2 diabetes mellitus.

Garcia-Roves, Pablo M

publication RETRACTED

Archives of physiology and biochemistry

2011 Volume 117, Issue 3, Page(s) 177–187

Abstract: Over the last decades, substantial progress has been made in defining the molecular events and relevant tissues controlling insulin action and the potential defects that lead to insulin resistance and later on Type 2 diabetes mellitus (T2DM). ... ...

Abstract	Over the last decades, substantial progress has been made in defining the molecular events and relevant tissues controlling insulin action and the potential defects that lead to insulin resistance and later on Type 2 diabetes mellitus (T2DM). Mitochondrial dysfunction has been postulated as a common mechanism implicated in the development of insulin resistance and T2DM aetiology. Since then there has been growing interest in this area of research and many studies have addressed whether mitochondrial function/dysfunction is implicated in the progression of T2DM or if it is just a consequence. Mitochondria are adjusted to the specific needs of the tissue and to the environmental interactions or pathophysiological state that it encounters. This review offers a current state of the subject in a tissue specific approach. We will focus our attention on skeletal muscle, liver, and white adipose tissue as the main insulin sensitive organs. Hypothalamic mitochondrial function will be also discussed.
MeSH term(s)	Adipose Tissue, White/metabolism ; Adipose Tissue, White/physiopathology ; Animals ; Diabetes Mellitus, Type 2/physiopathology ; Energy Metabolism ; Humans ; Hypothalamus/metabolism ; Hypothalamus/physiopathology ; Insulin/metabolism ; Insulin Resistance/physiology ; Liver/metabolism ; Liver/physiopathology ; Mitochondria/physiology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiopathology
Chemical Substances	Insulin
Language	English
Publishing date	2011-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Retracted Publication ; Review
ZDB-ID	1238320-x
ISSN	1744-4160 ; 1381-3455
ISSN (online)	1744-4160
ISSN	1381-3455
DOI	10.3109/13813455.2011.584538
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Article ; Online: Exercise-beyond skeletal muscle energy metabolism.

Garcia-Roves, Pablo M

Journal of applied physiology (Bethesda, Md. : 1985)

2010 Volume 108, Issue 1, Page(s) 224–4; author reply 226

MeSH term(s)	Animals ; Energy Metabolism/physiology ; Muscle Contraction/physiology ; Muscle, Skeletal/physiology ; Physical Conditioning, Animal/classification ; Physical Conditioning, Animal/standards ; Physiology/standards
Language	English
Publishing date	2010-01-08
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.01233.2009
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Article ; Online: Editorial:Dissecting the Role of Mitochondria in the Pathophysiology of Type-2 Diabetes and Obesity: Novel Concepts and Challenges.

Claret, Marc / Garcia-Roves, Pablo M

Current diabetes reviews

2016 Volume 13, Issue 4, Page(s) 337

MeSH term(s)	Animals ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Diabetes Mellitus, Type 2/physiopathology ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Degradation ; Mitochondrial Dynamics ; Obesity/epidemiology ; Obesity/metabolism ; Obesity/pathology ; Obesity/physiopathology ; Prevalence
Language	English
Publishing date	2016-02-28
Publishing country	United Arab Emirates
Document type	Editorial ; Introductory Journal Article
ISSN	1875-6417
ISSN (online)	1875-6417
DOI	10.2174/157339981304170725150725
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Article ; Online: Dietary Calanus oil recovers metabolic flexibility and rescues postischemic cardiac function in obese female mice.

Jansen, Kirsten M / Moreno, Sonia / Garcia-Roves, Pablo M / Larsen, Terje S

American journal of physiology. Heart and circulatory physiology

2019 Volume 317, Issue 2, Page(s) H290–H299

Abstract: The aim of this study was to find out whether dietary supplementation with Calanus oil (a novel marine oil) or infusion of exenatide (an incretin mimetic) could counteract obesity-induced alterations in myocardial metabolism and improve postischemic ... ...

Abstract	The aim of this study was to find out whether dietary supplementation with Calanus oil (a novel marine oil) or infusion of exenatide (an incretin mimetic) could counteract obesity-induced alterations in myocardial metabolism and improve postischemic recovery of left ventricular (LV) function. Female C57bl/6J mice received high-fat diet (HFD, 45% energy from fat) for 12 wk followed by 8-wk feeding with nonsupplemented HFD, HFD supplemented with 2% Calanus oil, or HFD plus exenatide infusion (10 µg·kg
MeSH term(s)	Animal Feed ; Animals ; Copepoda ; Disease Models, Animal ; Energy Metabolism ; Exenatide/administration & dosage ; Fatty Acids/metabolism ; Female ; Glucose/metabolism ; Incretins/administration & dosage ; Isolated Heart Preparation ; Mice, Inbred C57BL ; Myocardial Contraction ; Myocardial Reperfusion Injury/diet therapy ; Myocardial Reperfusion Injury/etiology ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/physiopathology ; Myocardium/metabolism ; Obesity/complications ; Oils/administration & dosage ; Oils/metabolism ; Recovery of Function ; Ventricular Function, Left ; Ventricular Pressure
Chemical Substances	Fatty Acids ; Incretins ; Oils ; Exenatide (9P1872D4OL) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-05-24
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00191.2019
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Article ; Online: The antioxidant l-Ergothioneine prevents cystine lithiasis in the Slc7a9

Mayayo-Vallverdú, Clara / López de Heredia, Miguel / Prat, Esther / González, Laura / Espino Guarch, Meritxell / Vilches, Clara / Muñoz, Lourdes / Asensi, Miguel A / Serra, Carmen / Llebaria, Amadeu / Casado, Mercedes / Artuch, Rafael / Garrabou, Gloria / Garcia-Roves, Pablo M / Pallardó, Federico V / Nunes, Virginia

Redox biology

2023 Volume 64, Page(s) 102801

Abstract: The high recurrence rate of cystine lithiasis observed in cystinuria patients highlights the need for new therapeutic options to address this chronic disease. There is growing evidence of an antioxidant defect in cystinuria, which has led to test ... ...

Abstract	The high recurrence rate of cystine lithiasis observed in cystinuria patients highlights the need for new therapeutic options to address this chronic disease. There is growing evidence of an antioxidant defect in cystinuria, which has led to test antioxidant molecules as new therapeutic approaches. In this study, the antioxidant l-Ergothioneine was evaluated, at two different doses, as a preventive and long-term treatment for cystinuria in the Slc7a9
MeSH term(s)	Animals ; Mice ; Ergothioneine/pharmacology ; Lithiasis/prevention & control ; Cystinuria/drug therapy ; Cystine ; Antioxidants/pharmacology ; Mice, Knockout ; Male ; Female ; Mice, Inbred C57BL ; Glutathione/metabolism ; Kidney/drug effects ; Kidney/metabolism ; Mitochondria/drug effects ; Oxidative Stress
Chemical Substances	Ergothioneine (BDZ3DQM98W) ; Cystine (48TCX9A1VT) ; Antioxidants ; Slc7a9 protein, mouse ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2023-06-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2023.102801
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Article ; Online: Energy substrate metabolism, mitochondrial structure and oxidative stress after cardiac ischemia-reperfusion in mice lacking UCP3.

Sánchez-Pérez, Patricia / Mata, Ana / Torp, May-Kristin / López-Bernardo, Elia / Heiestad, Christina M / Aronsen, Jan Magnus / Molina-Iracheta, Antonio / Jiménez-Borreguero, Luis J / García-Roves, Pablo / Costa, Ana S H / Frezza, Christian / Murphy, Michael P / Stenslokken, Kåre-Olav / Cadenas, Susana

Free radical biology & medicine

2023 Volume 205, Page(s) 244–261

Abstract: Myocardial ischemia-reperfusion (IR) injury may result in cardiomyocyte dysfunction. Mitochondria play a critical role in cardiomyocyte recovery after IR injury. The mitochondrial uncoupling protein 3 (UCP3) has been proposed to reduce mitochondrial ... ...

Abstract	Myocardial ischemia-reperfusion (IR) injury may result in cardiomyocyte dysfunction. Mitochondria play a critical role in cardiomyocyte recovery after IR injury. The mitochondrial uncoupling protein 3 (UCP3) has been proposed to reduce mitochondrial reactive oxygen species (ROS) production and to facilitate fatty acid oxidation. As both mechanisms might be protective following IR injury, we investigated functional, mitochondrial structural, and metabolic cardiac remodeling in wild-type mice and in mice lacking UCP3 (UCP3-KO) after IR. Results showed that infarct size in isolated perfused hearts subjected to IR ex vivo was larger in adult and old UCP3-KO mice than in equivalent wild-type mice, and was accompanied by higher levels of creatine kinase in the effluent and by more pronounced mitochondrial structural changes. The greater myocardial damage in UCP3-KO hearts was confirmed in vivo after coronary artery occlusion followed by reperfusion. S1QEL, a suppressor of superoxide generation from site I
MeSH term(s)	Mice ; Animals ; Superoxides/metabolism ; Myocardial Ischemia/metabolism ; Myocytes, Cardiac/metabolism ; Mitochondria/metabolism ; Oxidative Stress ; Myocardial Reperfusion Injury/genetics ; Myocardial Reperfusion Injury/metabolism ; Coronary Artery Disease/metabolism ; Energy Metabolism ; Ischemia/metabolism ; Reperfusion ; Fatty Acids/metabolism ; Infarction/complications ; Infarction/metabolism
Chemical Substances	Superoxides (11062-77-4) ; Fatty Acids
Language	English
Publishing date	2023-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2023.05.014
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Article ; Online: Chronic lymphocytic leukemia patient-derived xenografts recapitulate clonal evolution to Richter transformation.

Playa-Albinyana, Heribert / Arenas, Fabian / Royo, Romina / Giró, Ariadna / López-Oreja, Irene / Aymerich, Marta / López-Guerra, Mònica / Frigola, Gerard / Beà, Sílvia / Delgado, Julio / Garcia-Roves, Pablo M / Campo, Elías / Nadeu, Ferran / Colomer, Dolors

Leukemia

2023 Volume 38, Issue 3, Page(s) 557–569

Abstract: Chronic lymphocytic leukemia (CLL) is a B-cell neoplasm with a heterogeneous clinical behavior. In 5-10% of patients the disease transforms into a diffuse large-B cell lymphoma known as Richter transformation (RT), which is associated with dismal ... ...

Abstract	Chronic lymphocytic leukemia (CLL) is a B-cell neoplasm with a heterogeneous clinical behavior. In 5-10% of patients the disease transforms into a diffuse large-B cell lymphoma known as Richter transformation (RT), which is associated with dismal prognosis. Here, we aimed to establish patient-derived xenograft (PDX) models to study the molecular features and evolution of CLL and RT. We generated two PDXs by injecting CLL (PDX12) and RT (PDX19) cells into immunocompromised NSG mice. Both PDXs were morphologically and phenotypically similar to RT. Whole-genome sequencing analysis at different time points of the PDX evolution revealed a genomic landscape similar to RT tumors from both patients and uncovered an unprecedented RT subclonal heterogeneity and clonal evolution during PDX generation. In PDX12, the transformed cells expanded from a very small subclone already present at the CLL stage. Transcriptomic analysis of PDXs showed a high oxidative phosphorylation (OXPHOS) and low B-cell receptor (BCR) signaling similar to the RT in the patients. IACS-010759, an OXPHOS inhibitor, reduced proliferation, and circumvented resistance to venetoclax. In summary, we have generated new RT-PDX models, one of them from CLL cells that mimicked the evolution of CLL to RT uncovering intrinsic features of RT cells of therapeutical value.
MeSH term(s)	Humans ; Animals ; Mice ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Heterografts ; Lymphoma, Large B-Cell, Diffuse/genetics ; Lymphoma, Large B-Cell, Diffuse/pathology ; Clonal Evolution/genetics ; Prognosis ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology
Language	English
Publishing date	2023-11-28
Publishing country	England
Document type	Journal Article
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-023-02095-5
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