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Article ; Online: From Beats to Metabolism: the Heart at the Core of Interorgan Metabolic Cross Talk.

Romero-Becera, Rafael / Santamans, Ayelén M / Arcones, Alba C / Sabio, Guadalupe

2023 Volume 39, Issue 2, Page(s) 98–125

Abstract: The heart, once considered a mere blood pump, is now recognized as a multifunctional metabolic and endocrine organ. Its function is tightly regulated by various metabolic processes, at the same time it serves as an endocrine organ, secreting bioactive ... ...

Abstract	The heart, once considered a mere blood pump, is now recognized as a multifunctional metabolic and endocrine organ. Its function is tightly regulated by various metabolic processes, at the same time it serves as an endocrine organ, secreting bioactive molecules that impact systemic metabolism. In recent years, research has shed light on the intricate interplay between the heart and other metabolic organs, such as adipose tissue, liver, and skeletal muscle. The metabolic flexibility of the heart and its ability to switch between different energy substrates play a crucial role in maintaining cardiac function and overall metabolic homeostasis. Gaining a comprehensive understanding of how metabolic disorders disrupt cardiac metabolism is crucial, as it plays a pivotal role in the development and progression of cardiac diseases. The emerging understanding of the heart as a metabolic and endocrine organ highlights its essential contribution to whole body metabolic regulation and offers new insights into the pathogenesis of metabolic diseases, such as obesity, diabetes, and cardiovascular disorders. In this review, we provide an in-depth exploration of the heart's metabolic and endocrine functions, emphasizing its role in systemic metabolism and the interplay between the heart and other metabolic organs. Furthermore, emerging evidence suggests a correlation between heart disease and other conditions such as aging and cancer, indicating that the metabolic dysfunction observed in these conditions may share common underlying mechanisms. By unraveling the complex mechanisms underlying cardiac metabolism, we aim to contribute to the development of novel therapeutic strategies for metabolic diseases and improve overall cardiovascular health.
MeSH term(s)	Humans ; Diabetes Mellitus/metabolism ; Adipose Tissue/metabolism ; Homeostasis ; Metabolic Diseases/metabolism ; Signal Transduction
Language	English
Publishing date	2023-12-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2158667-6
ISSN	1548-9221 ; 1548-9213
ISSN (online)	1548-9221
ISSN	1548-9213
DOI	10.1152/physiol.00018.2023
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Article ; Online: Brain JNK and metabolic disease.

Nogueiras, Rubén / Sabio, Guadalupe

Diabetologia

2020 Volume 64, Issue 2, Page(s) 265–274

Abstract: Obesity, which has long since reached epidemic proportions worldwide, is associated with long-term stress to a variety of organs and results in diseases including type 2 diabetes. In the brain, overnutrition induces hypothalamic stress associated with ... ...

Abstract	Obesity, which has long since reached epidemic proportions worldwide, is associated with long-term stress to a variety of organs and results in diseases including type 2 diabetes. In the brain, overnutrition induces hypothalamic stress associated with the activation of several signalling pathways, together with central insulin and leptin resistance. This central action of nutrient overload appears very rapidly, suggesting that nutrition-induced hypothalamic stress is a major upstream initiator of obesity and associated diseases. The cellular response to nutrient overload includes the activation of the stress-activated c-Jun N-terminal kinases (JNKs) JNK1, JNK2 and JNK3, which are widely expressed in the brain. Here, we review recent findings on the regulation and effects of these kinases, with particular focus on the hypothalamus, a key brain region in the control of energy and glucose homeostasis. JNK1 blocks the hypothalamic-pituitary-thyroid axis, reducing energy expenditure and promoting obesity. Recently, opposing roles have been identified for JNK1 and JNK3 in hypothalamic agouti gene-related protein (AgRP) neurons: while JNK1 activation in AgRP neurons induces feeding and weight gain and impairs insulin and leptin signalling, JNK3 (also known as MAPK10) deletion in the same neuronal population produces very similar effects. The opposing roles of these kinases, and the unknown role of hypothalamic JNK2, reflect the complexity of JNK biology. Future studies should address the specific function of each kinase, not only in different neuronal subsets, but also in non-neuronal cells in the central nervous system. Decoding the puzzle of brain stress kinases will help to define the central stimuli and mechanisms implicated in the control of energy balance. Graphical abstract.
MeSH term(s)	Agouti-Related Protein/metabolism ; Animals ; Brain/cytology ; Brain/metabolism ; Endoplasmic Reticulum Stress ; Energy Metabolism/physiology ; Feeding Behavior/physiology ; Glucose/metabolism ; Humans ; Hypothalamo-Hypophyseal System/metabolism ; Hypothalamus/cytology ; Hypothalamus/metabolism ; Insulin/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Leptin/metabolism ; Metabolic Diseases/metabolism ; Mitogen-Activated Protein Kinase 10/metabolism ; Mitogen-Activated Protein Kinase 8/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism ; Neurons/cytology ; Neurons/metabolism ; Obesity/metabolism ; Thyroid Gland/metabolism ; Weight Gain/physiology
Chemical Substances	Agouti-Related Protein ; Insulin ; Leptin ; Mitogen-Activated Protein Kinase 10 (EC 2.7.1.-) ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-11-16
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-020-05327-w
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Article: Circadian Clock and Liver Cancer.

Crespo, María / Leiva, Magdalena / Sabio, Guadalupe

Cancers

2021 Volume 13, Issue 14

Abstract: Circadian clocks control several homeostatic processes in mammals through internal molecular mechanisms. Chronic perturbation of circadian rhythms is associated with metabolic diseases and increased cancer risk, including liver cancer. The hepatic ... ...

Abstract	Circadian clocks control several homeostatic processes in mammals through internal molecular mechanisms. Chronic perturbation of circadian rhythms is associated with metabolic diseases and increased cancer risk, including liver cancer. The hepatic physiology follows a daily rhythm, driven by clock genes that control the expression of several proteins involved in distinct metabolic pathways. Alteration of the liver clock results in metabolic disorders, such as non-alcoholic fatty liver diseases (NAFLD) and impaired glucose metabolism, that can trigger the activation of oncogenic pathways, inducing spontaneous hepatocarcinoma (HCC). In this review, we provide an overview of the role of the liver clock in the metabolic and oncogenic changes that lead to HCC and discuss new potentially useful targets for prevention and management of HCC.
Language	English
Publishing date	2021-07-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13143631
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Article ; Online: DIDO is necessary for the adipogenesis that promotes diet-induced obesity.

García-López, María Ángeles / Mora, Alfonso / Corrales, Patricia / Pons, Tirso / Sánchez de Diego, Ainhoa / Talavera Gutiérrez, Amaia / van Wely, Karel H M / Medina-Gómez, Gema / Sabio, Guadalupe / Martínez-A, Carlos / Fischer, Thierry

Proceedings of the National Academy of Sciences of the United States of America

2024 Volume 121, Issue 3, Page(s) e2300096121

Abstract: The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue ( ... ...

Abstract	The prevalence of overweight and obesity continues to rise in the population worldwide. Because it is an important predisposing factor for cancer, cardiovascular diseases, diabetes mellitus, and COVID-19, obesity reduces life expectancy. Adipose tissue (AT), the main fat storage organ with endocrine capacity, plays fundamental roles in systemic metabolism and obesity-related diseases. Dysfunctional AT can induce excess or reduced body fat (lipodystrophy).
MeSH term(s)	Animals ; Mice ; Adipogenesis/genetics ; Cell Differentiation ; Diet ; Lipodystrophy ; Obesity/genetics ; Overweight
Chemical Substances	Dido protein, mouse
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2300096121
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Article ; Online: The role of stress kinases in metabolic disease.

Nikolic, Ivana / Leiva, Magdalena / Sabio, Guadalupe

Nature reviews. Endocrinology

2020 Volume 16, Issue 12, Page(s) 697–716

Abstract: Obesity is a health condition that has reached pandemic levels and is implicated in the development and progression of type 2 diabetes mellitus, cancer and heart failure. A key characteristic of obesity is the activation of stress-activated protein ... ...

Abstract	Obesity is a health condition that has reached pandemic levels and is implicated in the development and progression of type 2 diabetes mellitus, cancer and heart failure. A key characteristic of obesity is the activation of stress-activated protein kinases (SAPKs), such as the p38 and JNK stress kinases, in several organs, including adipose tissue, liver, skeletal muscle, immune organs and the central nervous system. The correct timing, intensity and duration of SAPK activation contributes to cellular metabolic adaptation. By contrast, uncontrolled SAPK activation has been proposed to contribute to the complications of obesity. The stress kinase signalling pathways have therefore been identified as potential targets for the development of novel therapeutic approaches for metabolic syndrome. The past few decades have seen intense research efforts to determine how these kinases are regulated in a cell-specific manner and to define their contribution to the development of obesity and insulin resistance. Several studies have uncovered new and unexpected functions of the non-classical members of both pathways. Here, we provide an overview of the role of SAPKs in metabolic control and highlight important discoveries in the field.
MeSH term(s)	Animals ; Humans ; Metabolic Diseases/metabolism ; Obesity/metabolism ; Protein Kinases/metabolism ; Stress, Physiological
Chemical Substances	Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2020-10-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-020-00418-5
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Zs.MG 93: Show issues

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Article ; Online: Unicentric Castleman's disease mimicking an hilar lung cancer.

Fuentes, Guadalupe Carrasco / López, Sebastian Sevilla / González, Adela Sabio / Cerro, Antonio J Bravo

Cirugia espanola

2022 Volume 101, Issue 4, Page(s) 298–300

MeSH term(s)	Humans ; Castleman Disease/diagnosis ; Castleman Disease/surgery ; Mediastinal Diseases ; Lung Neoplasms/diagnosis
Language	English
Publishing date	2022-06-02
Publishing country	Spain
Document type	Case Reports
ISSN	2173-5077
ISSN (online)	2173-5077
DOI	10.1016/j.cireng.2022.06.004
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Article ; Online: Stress kinases in the development of liver steatosis and hepatocellular carcinoma.

Cicuéndez, Beatriz / Ruiz-Garrido, Irene / Mora, Alfonso / Sabio, Guadalupe

Molecular metabolism

2021 Volume 50, Page(s) 101190

Abstract: Non-alcoholic fatty liver disease (NAFLD) is an important component of metabolic syndrome and one of the most prevalent liver diseases worldwide. This disorder is closely linked to hepatic insulin resistance, lipotoxicity, and inflammation. Although the ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is an important component of metabolic syndrome and one of the most prevalent liver diseases worldwide. This disorder is closely linked to hepatic insulin resistance, lipotoxicity, and inflammation. Although the mechanisms that cause steatosis and chronic liver injury in NAFLD remain unclear, a key component of this process is the activation of stress-activated kinases (SAPKs), including p38 and JNK in the liver and immune system. This review summarizes findings which indicate that the dysregulation of stress kinases plays a fundamental role in the development of steatosis and are important players in inducing liver fibrosis. To avoid the development of steatohepatitis and liver cancer, SAPK activity must be tightly regulated not only in the hepatocytes but also in other tissues, including cells of the immune system. Possible cellular mechanisms of SAPK actions are discussed.
MeSH term(s)	Animals ; Autophagy/drug effects ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Disease Models, Animal ; Humans ; Insulin Resistance ; JNK Mitogen-Activated Protein Kinases/metabolism ; Liver/pathology ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; MAP Kinase Signaling System ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology ; Protective Agents/pharmacology ; Protective Agents/therapeutic use ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Protective Agents ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2021-02-13
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2021.101190
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Article ; Online: Stress kinases in the development of liver steatosis and hepatocellular carcinoma

Beatriz Cicuéndez / Irene Ruiz-Garrido / Alfonso Mora / Guadalupe Sabio

Molecular Metabolism, Vol 50, Iss , Pp 101190- (2021)

2021

Abstract	Non-alcoholic fatty liver disease (NAFLD) is an important component of metabolic syndrome and one of the most prevalent liver diseases worldwide. This disorder is closely linked to hepatic insulin resistance, lipotoxicity, and inflammation. Although the mechanisms that cause steatosis and chronic liver injury in NAFLD remain unclear, a key component of this process is the activation of stress-activated kinases (SAPKs), including p38 and JNK in the liver and immune system. This review summarizes findings which indicate that the dysregulation of stress kinases plays a fundamental role in the development of steatosis and are important players in inducing liver fibrosis. To avoid the development of steatohepatitis and liver cancer, SAPK activity must be tightly regulated not only in the hepatocytes but also in other tissues, including cells of the immune system. Possible cellular mechanisms of SAPK actions are discussed.
Keywords	SAPK ; JNK ; p38 ; Steatosis ; Hepatocarcinoma ; Metabolism ; Internal medicine ; RC31-1245
Subject code	610
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: p38 MAPK Pathway in the Heart: New Insights in Health and Disease.

Romero-Becerra, Rafael / Santamans, Ayelén M / Folgueira, Cintia / Sabio, Guadalupe

International journal of molecular sciences

2020 Volume 21, Issue 19

Abstract: The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac ... ...

Abstract	The p38 mitogen-activated kinase (MAPK) family controls cell adaptation to stress stimuli. p38 function has been studied in depth in relation to cardiac development and function. The first isoform demonstrated to play an important role in cardiac development was p38α; however, all p38 family members are now known to collaborate in different aspects of cardiomyocyte differentiation and growth. p38 family members have been proposed to have protective and deleterious actions in the stressed myocardium, with the outcome of their action in part dependent on the model system under study and the identity of the activated p38 family member. Most studies to date have been performed with inhibitors that are not isoform-specific, and, consequently, knowledge remains very limited about how the different p38s control cardiac physiology and respond to cardiac stress. In this review, we summarize the current understanding of the role of the p38 pathway in cardiac physiology and discuss recent advances in the field.
MeSH term(s)	Animals ; Arrhythmias, Cardiac/metabolism ; Cardiomegaly/metabolism ; Heart Failure/metabolism ; Humans ; Isoenzymes/antagonists & inhibitors ; Isoenzymes/metabolism ; MAP Kinase Signaling System/drug effects ; Myocardium/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Regeneration/physiology ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Treatment Outcome ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Isoenzymes ; Protein Kinase Inhibitors ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2020-10-08
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/ijms21197412
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Article: Title: p38δ Regulates IL6 Expression Modulating ERK Phosphorylation in Preadipocytes.

Díaz-Chamorro, Selene / Garrido-Jiménez, Sergio / Barrera-López, Juan Francisco / Mateos-Quirós, Clara María / Cumplido-Laso, Guadalupe / Lorenzo, María Jesús / Román, Ángel Carlos / Bernardo, Edgar / Sabio, Guadalupe / Carvajal-González, José María / Centeno, Francisco

Frontiers in cell and developmental biology

2022 Volume 9, Page(s) 708844

Abstract: IL6 is an essential cytokine in metabolism regulation and for intercommunication among different organs and tissues. IL6 produced by different tissues has different functions and therefore it is very important to understand the mechanism of its ... ...

Abstract	IL6 is an essential cytokine in metabolism regulation and for intercommunication among different organs and tissues. IL6 produced by different tissues has different functions and therefore it is very important to understand the mechanism of its expression in adipose tissue. In this work we demonstrated that IL6 expression in mouse preadipocytes, like in human, is partially dependent on Wnt5a and JNK. Using mouse preadipocytes lacking each one of the p38 SAPK family members, we have shown that IL6 expression is also p38γ and p38δ dependent. In fact, the lack of some of these two kinases increases IL6 expression without altering that of Wnt5a. Moreover, we show that the absence of p38δ promotes greater ERK1/2 phosphorylation in a MEK1/2 independent manner, and that this increased ERK1/2 phosphorylation state is contributing to the higher IL6 expression in p38δ
Language	English
Publishing date	2022-01-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.708844
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