María J. Vázquez

Hospital Universitario Reina Sofía

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Co-Authors

Carlos Diéguez

Universidade de Santiago de Compostela

Manuel Tena‐Sempere

Hospital Universitario Reina Sofía

Miguel López

Instituto de Investigación Sanitaria de Santiago

Rubén Nogueiras

Center for Research in Molecular Medicine and Chronic Diseases

Francisco Ruíz-Pino

Instituto de Salud Carlos III

Juan Roa

Instituto Maimónides de Investigación Biomédica de Córdoba

Francisco Gaytán

University of Córdoba

Juan M. Castellano

University of Córdoba

Leonor Pinilla

Instituto de Salud Carlos III

Miguel A. Sánchez-Garrido

Instituto de Salud Carlos III

Cooperative Institutions

Instituto de Salud Carlos III

103

Centro de Investigación Biomédica en Red

University of Córdoba

Instituto Maimónides de Investigación Biomédica de Córdoba

Hospital Universitario Reina Sofía

Universidade de Santiago de Compostela

Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition

Cordoba University

Instituto de Investigación Sanitaria de Santiago

Center for Research in Molecular Medicine and Chronic Diseases

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Hypothalamic melanin-concentrating hormone influences liver and adipose lipid metabolism

Endocrine Abstracts (2013)

Mónica Imbernón Daniel Beiroa María J. Vázquez Donald A. Morgan Christelle Veyrat‐Durebex

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Melanin-concentrating hormone

Lipogenesis

10.1530/endoabs.32.p681

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Ghrelin effects on neuropeptides in the rat hypothalamus depend on fatty acid metabolism actions on BSX but not on gender

The FASEB Journal (2010)

Ricardo Lage María J. Vázquez Luis Varela Asish K. Saha Antonio Vidal‐Puig

The orexigenic effect of ghrelin is mediated by neuropeptide Y (NPY) and agouti-related protein (AgRP) in the hypothalamic arcuate nucleus (ARC). Recent evidence also indicates that ghrelin promotes feeding through a mechanism involving activation of hypothalamic AMP-activated protein kinase (AMPK) and inactivation of acetyl-CoA carboxylase and fatty acid synthase (FAS). This results in decreased hypothalamic levels of malonyl-CoA, increased carnitine palmitoyltransferase 1 (CPT1) activity, and mitochondrial production of reactive oxygen species. We evaluated whether these molecular events are part of a unique signaling cascade or whether they represent alternative pathways mediating the orexigenic effect of ghrelin. Moreover, we examined the gender dependency of these mechanisms, because recent evidence has proposed that ghrelin orexigenic effect is reduced in female rats. We studied in both genders the effect of ghrelin on the expression of AgRP and NPY, as well as their transcription factors: cAMP response-element binding protein (CREB and its phosphorylated form, pCREB), forkhead box O1 (FoxO1 and its phosphorylated form, pFoxO1), and brain-specific homeobox transcription factor (BSX). In addition, to establish a mechanistic link between ghrelin, fatty acid metabolism, and neuropeptides, we evaluated the effect of ghrelin after blockage of hypothalamic fatty acid β oxidation, by using the CPT1 inhibitor etomoxir. Ghrelin-induced changes in the AMPK-CPT1 pathway are associated with increased levels of AgRP and NPY mRNA expression through modulation of BSX, pCREB, and FoxO1, as well as decreased expression of endoplasmic reticulum (ER) stress markers in a gender-independent manner. In addition, blockage of hypothalamic fatty acid β oxidation prevents the ghrelin-promoting action on AgRP and NPY mRNA expression, also in a gender-independent manner. Notably, this effect is associated with decreased BSX expression and reduced food intake. Overall, our data suggest that BSX integrates changes in neuronal metabolic status with ARC-derived neuropeptides in a gender-independent manner.—Lage, R., Vazquez, M. J., Varela, L., Saha, A. K., Vidal-Puig, A., Nogueiras, R., Diéguez, C., López, M. Ghrelin effects on neuropeptides in the rat hypothalamus depend on fatty acid metabolism actions on BSX but not on gender. FASEB J. 24, 2670–2679 (2010). www.fasebj.org

Orexigenic

10.1096/fj.09-150672

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Citations (118)

The Central Sirtuin 1/p53 Pathway Is Essential for the Orexigenic Action of Ghrelin

Diabetes (2011)

D Velasquez Gloria Martínez Amparo Romero María J. Vázquez Kátia Da Boit

Ghrelin is a stomach-derived peptide that increases food intake through the activation of hypothalamic AMP-activated protein kinase (AMPK). However, the molecular mechanisms initiated by the activation of the ghrelin receptor, which in turn lead to AMPK activation, remain unclear. Sirtuin 1 (SIRT1) is a deacetylase activated in response to calorie restriction that acts through the tumor suppressor gene p53. We tested the hypothesis that the central SIRT1/p53 pathway might be mediating the orexigenic action of ghrelin.SIRT1 inhibitors, such as Ex527 and sirtinol, and AMPK activators, such as AICAR, were administered alongside ghrelin in the brain of rats and mice (wild-type versus p53 knockout [KO]). Their hypothalamic effects on lipid metabolism and changes in transcription factors and neuropeptides were assessed by Western blot and in situ hybridization.The central pretreatment with Ex527, a potent SIRT1 inhibitor, blunted the ghrelin-induced food intake in rats. Mice lacking p53, a target of SIRT1 action, failed to respond to ghrelin in feeding behavior. Ghrelin failed to phosphorylate hypothalamic AMPK when rats were pretreated with Ex527, as it did in p53 KO mice. It is noteworthy that the hypothalamic SIRT1/p53 pathway seems to be specific for mediating the orexigenic action of ghrelin, because central administration of AICAR, a potent AMPK activator, increased food intake in p53 KO mice. Finally, blockade of the central SIRT1 pathway did not modify ghrelin-induced growth hormone secretion.Ghrelin specifically triggers a central SIRT1/p53 pathway that is essential for its orexigenic action, but not for the release of growth hormone.

Orexigenic

Sirtuin 1

Obestatin

10.2337/db10-0802

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Citations (153)

Central GLP-1 Actions on Energy Metabolism

Vitamins and hormones (2010)

D Velasquez Daniel Beiroa María J. Vázquez Amparo Romero Miguel López

Carbohydrate Metabolism

Nutrient Sensing

10.1016/b978-0-12-381517-0.00011-4

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Citations (8)

Neonatal events, such as androgenization and postnatal overfeeding, modify the response to ghrelin

Scientific Reports (2014)

Marta G. Novelle María J. Vázquez Kátia da Boit Martinello Miguel A. Sánchez-Garrido Manuel Tena‐Sempere

Abstract It is currently accepted that ambient, non-genetic factors influence perinatal development and evoke structural and functional changes that may persist throughout life. Overfeeding and androgenization after birth are two of these key factors that could result in “metabolic imprinting” of neuronal circuits early in life and, thereby, increase the body weight homeostatic “set point”, stimulate appetite and result in obesity. Our aim was to determine the influence of these obesogenic factors on the response to ghrelin. We observed the expected orexigenic effect of ghrelin regardless of the nutritional or hormonal manipulations to which the animals were subjected to at early postnatal development and this effect remained intact at later stages of development. In fact, ghrelin responses increased significantly when the animals were subjected to one of the two manipulations, but not when both were combined. An increased response to ghrelin could explain the obese phenotype displayed by individuals with modified perinatal environment.

Orexigenic

10.1038/srep04855

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Citations (9)

Ghrelin neutralization during fasting-refeeding cycle impairs the recuperation of body weight and alters hepatic energy metabolism

Molecular and Cellular Endocrinology (2011)

Susana Sangiao‐Alvarellos Steffen Helmling María J. Vázquez Sven Klußmann Fernando Cordido

Refeeding syndrome

10.1016/j.mce.2011.01.010

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Citations (23)

Hypothalamic SIRT1-mediated regulation of the hormonal trigger of ovulation and its repression in energy deficit

Metabolism (2024)

María J. Vázquez Silvia Daza‐Dueñas Inmaculada Velasco Francisco Ruíz-Pino María J. Sanchez-Tapia

Female reproduction is highly sensitive to body energy stores; persistent energy deficit, as seen in anorexia or strenuous exercise, is known to suppress ovulation via ill-defined mechanisms. We report herein that hypothalamic SIRT1, a key component of the epigenetic machinery that links nutritional status and puberty onset via modulation of Kiss1, plays a critical role in the control of the preovulatory surge of gonadotropins, i.e., the hormonal trigger of ovulation, and its repression by conditions of energy deficit. Kiss1 neurons in the preoptic area, with proven roles in the control of ovulation, express Sirt1 mRNA. Reciprocal changes in hypothalamic SIRT1 content and Kiss1 expression were observed during the pre-ovulatory phase in adult female rats. Central activation of SIRT1 reduced Kiss1 expression in the rostral hypothalamus, and attenuated the preovulatory surge, while blockade of central SIRT1 augmented it. Conditions of energy deficit enhanced hypothalamic SIRT1 activity and caused suppression of the pre-ovulatory surge and ovulation, which could be rescued by central SIRT1 inhibition. In turn, virogenetic induction of SIRT1 in rostral hypothalamic Kiss1 neurons in adult female mice disrupted ovarian cyclicity and suppressed reproductive indices, despite preserved body weight. Our data document the prominent function of hypothalamic SIRT1 as a key modulator of Kiss1 neurons and the hormonal surge driving ovulation in adulthood, with a major role in its inhibition during conditions of energy insufficiency.

Preoptic area

10.1016/j.metabol.2024.156125

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Central Ceramide Signaling Mediates Obesity-Induced Precocious Puberty

Cell Metabolism (2020)

Violeta Heras Juan M. Castellano Daniela Fernandois Inmaculada Velasco Elvira Rodríguez-Vázquez

Delayed puberty

Kisspeptin

10.1016/j.cmet.2020.10.001

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Citations (64)

Blockage of the Neonatal Leptin Surge Affects the Gene Expression of Growth Factors, Glial Proteins, and Neuropeptides Involved in the Control of Metabolism and Reproduction in Peripubertal Male and Female Rats

Endocrinology (2015)

Virginia Mela Francisca Díaz Ana Belén López-Rodríguez María J. Vázquez Arieh Gertler

Leptin (Lep) is important in the development of neuroendocrine circuits involved in metabolic control. Because both Lep and metabolism influence pubertal development, we hypothesized that early changes in Lep signaling could also modulate hypothalamic (HT) systems involved in reproduction. We previously demonstrated that a single injection of a Lep antagonist (Antag) on postnatal day (PND)9, coincident with the neonatal Lep peak, induced sexually dimorphic modifications in trophic factors and markers of cell turnover and neuronal maturation in the HT on PND13. Here, our aim was to investigate whether the alterations induced by Lep antagonism persist into puberty. Accordingly, male and female rats were treated with a pegylated super Lep Antag from PND5 to PND9 and killed just before the normal appearance of external signs of puberty (PND33 in females and PND43 in males). There was no effect on body weight, but in males food intake increased, subcutaneous adipose tissue decreased and HT neuropeptide Y and Agouti-related peptide mRNA levels were reduced, with no effect in females. In both sexes, the Antag increased HT mRNA levels of the kisspeptin receptor, G protein-coupled recepter 54 (Gpr54). Expression of the Lep receptor, trophic factors, and glial markers were differently affected in the HT of peripubertal males and females. Lep production in adipose tissue was decreased in Antag-treated rats of both sexes, with production of other cytokines being differentially regulated between sexes. In conclusion, in addition to the long-term effects on metabolism, changes in neonatal Lep levels modifies factors involved in reproduction that could possibly affect sexual maturation.

Kisspeptin

Leptin receptor

10.1210/en.2014-1981

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Citations (19)

Efficacy of chronic hepatitis C therapy with pegylated interferon and ribavirin in patients on methadone maintenance treatment

European Journal of Clinical Microbiology & Infectious Diseases (2011)

Karin Neukam J. A. Mira Isabel Gilabert Evangelina Claro María J. Vázquez

Pegylated interferon

Hepatitis C

Methadone maintenance

10.1007/s10096-011-1433-5

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Citations (6)