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17 results on '"Rodríguez-Cuenca, Sergio"'

1. Defective extracellular matrix remodeling in brown adipose tissue is associated with fibro-inflammation and reduced diet-induced thermogenesis

Author

Pellegrinelli, Vanessa, Figueroa-Juárez, Elizabeth, Samuelson, Isabella, U-Din, Mueez, Rodriguez-Fdez, Sonia, Virtue, Samuel, Leggat, Jennifer, Çubuk, Cankut, Peirce, Vivian J., Niemi, Tarja, Campbell, Mark, Rodriguez-Cuenca, Sergio, Blázquez, Joaquin Dopazo, Carobbio, Stefania, Virtanen, Kirsi A., and Vidal-Puig, Antonio

Published
2023
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2. Defective extracellular matrix remodeling in brown adipose tissue is associated with fibro-inflammation and reduced diet-induced thermogenesis

Author

Wellcome Trust, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Academy of Finland, Paulo Foundation, Finnish Cultural Foundation, Turku University Central Hospital, European Commission, Fundación Ramón Areces, Wellcome Sanger Institute, Pellegrinelli, Vanessa, Figueroa-Juárez, Elizabeth, Samuelson, Isabella, U-Din, Mueez, Rodríguez-Fdez, Sonia, Virtue, Samuel, Leggat, Jennifer, Çubuk, Cankut, Peirce, Vivian J., Niemi, Tarja, Campbell, Mark, Rodríguez-Cuenca, Sergio, Dopazo, Joaquín, Carobbio, Stefania, Virtanen, Kirsi A., Vidal-Puig, Antonio, Wellcome Trust, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Academy of Finland, Paulo Foundation, Finnish Cultural Foundation, Turku University Central Hospital, European Commission, Fundación Ramón Areces, Wellcome Sanger Institute, Pellegrinelli, Vanessa, Figueroa-Juárez, Elizabeth, Samuelson, Isabella, U-Din, Mueez, Rodríguez-Fdez, Sonia, Virtue, Samuel, Leggat, Jennifer, Çubuk, Cankut, Peirce, Vivian J., Niemi, Tarja, Campbell, Mark, Rodríguez-Cuenca, Sergio, Dopazo, Joaquín, Carobbio, Stefania, Virtanen, Kirsi A., and Vidal-Puig, Antonio

Abstract

The relevance of extracellular matrix (ECM) remodeling is reported in white adipose tissue (AT) and obesity-related dysfunctions, but little is known about the importance of ECM remodeling in brown AT (BAT) function. Here, we show that a time course of high-fat diet (HFD) feeding progressively impairs diet-induced thermogenesis concomitantly with the development of fibro-inflammation in BAT. Higher markers of fibro-inflammation are associated with lower cold-induced BAT activity in humans. Similarly, when mice are housed at thermoneutrality, inactivated BAT features fibro-inflammation. We validate the pathophysiological relevance of BAT ECM remodeling in response to temperature challenges and HFD using a model of a primary defect in the collagen turnover mediated by partial ablation of the Pepd prolidase. Pepd-heterozygous mice display exacerbated dysfunction and BAT fibro-inflammation at thermoneutrality and in HFD. Our findings show the relevance of ECM remodeling in BAT activation and provide a mechanism for BAT dysfunction in obesity.

Published
2023

5. Consequences of long-term oral administration of the mitochondria-targeted antioxidant MitoQ to wild-type mice

Author

Rodriguez-Cuenca, Sergio, Cochemé, Helena M., Logan, Angela, Abakumova, Irina, Prime, Tracy A., Rose, Claudia, Vidal-Puig, Antonio, Smith, Anthony C., Rubinsztein, David C., Fearnley, Ian M., Jones, Bruce A., Pope, Simon, Heales, Simon J.R., Lam, Brian Y.H., Neogi, Sudeshna Guha, McFarlane, Ian, James, Andrew M., Smith, Robin A.J., and Murphy, Michael P.

Published
2010
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7. Hypothalamic Fatty Acid Metabolism Mediates the Orexigenic Action of Ghrelin

Author

López, Miguel, Lage, Ricardo, Saha, Asish K., Pérez-Tilve, Diego, Vázquez, María J., Varela, Luis, Sangiao-Alvarellos, Susana, Tovar, Sulay, Raghay, Kawtar, Rodríguez-Cuenca, Sergio, Deoliveira, Rosangela M., Castañeda, Tamara, Datta, Rakesh, Dong, Jesse Z., Culler, Michael, Sleeman, Mark W., Álvarez, Clara V., Gallego, Rosalía, Lelliott, Christopher J., Carling, David, Tschöp, Matthias H., Diéguez, Carlos, and Vidal-Puig, Antonio

Published
2008
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11. Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance

Author

López, Miguel, Varela, Luis, Vázquez, María J, Rodríguez-Cuenca, Sergio, González, Carmen R., Velagapudi, Vidya R., Morgan, Donald A., Schoenmakers, Erik, Agassandian, Khristofor, Lage, Ricardo, Martínez de Morentin, Pablo Blanco, Tovar, Sulay, Nogueiras, Rubén, Carling, David, Lelliott, Christopher, Gallego, Rosalía, Oresic, Matej, Chatterjee, Krishna, Saha, Asish K, Rahmouni, Kamal, Diéguez, Carlos, Vidal-Puig, Antonio, López, Miguel, Varela, Luis, Vázquez, María J, Rodríguez-Cuenca, Sergio, González, Carmen R., Velagapudi, Vidya R., Morgan, Donald A., Schoenmakers, Erik, Agassandian, Khristofor, Lage, Ricardo, Martínez de Morentin, Pablo Blanco, Tovar, Sulay, Nogueiras, Rubén, Carling, David, Lelliott, Christopher, Gallego, Rosalía, Oresic, Matej, Chatterjee, Krishna, Saha, Asish K, Rahmouni, Kamal, Diéguez, Carlos, and Vidal-Puig, Antonio

Abstract

Thyroid hormones have widespread cellular effects; however it is unclear whether their effects on the central nervous system (CNS) contribute to global energy balance. Here we demonstrate that either whole-body hyperthyroidism or central administration of triiodothyronine (T3) decreases the activity of hypothalamic AMP-activated protein kinase (AMPK), increases sympathetic nervous system (SNS) activity and upregulates thermogenic markers in brown adipose tissue (BAT). Inhibition of the lipogenic pathway in the ventromedial nucleus of the hypothalamus (VMH) prevents CNS-mediated activation of BAT by thyroid hormone and reverses the weight loss associated with hyperthyroidism. Similarly, inhibition of thyroid hormone receptors in the VMH reverses the weight loss associated with hyperthyroidism. This regulatory mechanism depends on AMPK inactivation, as genetic inhibition of this enzyme in the VMH of euthyroid rats induces feeding-independent weight loss and increases expression of thermogenic markers in BAT. These effects are reversed by pharmacological blockade of the SNS. Thus, thyroid hormone-induced modulation of AMPK activity and lipid metabolism in the hypothalamus is a major regulator of whole-body energy homeostasis., Funding agencies:UK Medical Research Council G0802051

Published
2010
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12. Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance

Author

López, Miguel, primary, Varela, Luis, additional, Vázquez, María J, additional, Rodríguez-Cuenca, Sergio, additional, González, Carmen R, additional, Velagapudi, Vidya R, additional, Morgan, Donald A, additional, Schoenmakers, Erik, additional, Agassandian, Khristofor, additional, Lage, Ricardo, additional, de Morentin, Pablo Blanco Martínez, additional, Tovar, Sulay, additional, Nogueiras, Rubén, additional, Carling, David, additional, Lelliott, Christopher, additional, Gallego, Rosalía, additional, Orešič, Matej, additional, Chatterjee, Krishna, additional, Saha, Asish K, additional, Rahmouni, Kamal, additional, Diéguez, Carlos, additional, and Vidal-Puig, Antonio, additional

Published
2010
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17. Identification of Novel Type 2 Diabetes Candidate Genes Involved in the Crosstalk between the Mitochondrial and the Insulin Signaling Systems

Author

Mercader, Josep M., Puiggros, Montserrat, Segrè, Ayellet V., Planet, Evarist, Sorianello, Eleonora, Sebastian, David, Rodriguez-Cuenca, Sergio, Ribas, Vicent, Bonàs-Guarch, Sílvia, Draghici, Sorin, Yang, Chenjing, Mora, Sílvia, Vidal-Puig, Antoni, Dupuis, Josée, Zorzano, Antonio, Torrents, David, and Florez, Jose Carlos

Subjects
Biology, Computational Biology, Genomics, Functional Genomics, Metabolic Networks, Signaling Networks, Systems Biology, Genetics, Genome-Wide Association Studies
Abstract

Type 2 Diabetes (T2D) is a highly prevalent chronic metabolic disease with strong co-morbidity with obesity and cardiovascular diseases. There is growing evidence supporting the notion that a crosstalk between mitochondria and the insulin signaling cascade could be involved in the etiology of T2D and insulin resistance. In this study we investigated the molecular basis of this crosstalk by using systems biology approaches. We combined, filtered, and interrogated different types of functional interaction data, such as direct protein–protein interactions, co-expression analyses, and metabolic and signaling dependencies. As a result, we constructed the mitochondria-insulin (MITIN) network, which highlights 286 genes as candidate functional linkers between these two systems. The results of internal gene expression analysis of three independent experimental models of mitochondria and insulin signaling perturbations further support the connecting roles of these genes. In addition, we further assessed whether these genes are involved in the etiology of T2D using the genome-wide association study meta-analysis from the DIAGRAM consortium, involving 8,130 T2D cases and 38,987 controls. We found modest enrichment of genes associated with T2D amongst our linker genes (p = 0.0549), including three already validated T2D SNPs and 15 additional SNPs, which, when combined, were collectively associated to increased fasting glucose levels according to MAGIC genome wide meta-analysis (p = 8.12×10−5). This study highlights the potential of combining systems biology, experimental, and genome-wide association data mining for identifying novel genes and related variants that increase vulnerability to complex diseases.

Published
2012
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