Ismael González‐García

Center for Research in Molecular Medicine and Chronic Diseases

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Miguel López

Instituto de Investigación Sanitaria de Santiago

Carlos Diéguez

Universidade de Santiago de Compostela

Rubén Nogueiras

Center for Research in Molecular Medicine and Chronic Diseases

Cristina García‐Cáceres

Helmholtz Zentrum München

Manuel Tena‐Sempere

Hospital Universitario Reina Sofía

Johan Fernø

Haukeland University Hospital

Cristina Contreras

Universidad Complutense de Madrid

Tim Gruber

Van Andel Institute

ÁE

Ánxela Estévez‐Salguero

Center for Research in Molecular Medicine and Chronic Diseases

Edward Milbank

Center for Research in Molecular Medicine and Chronic Diseases

Cooperative Institutions

Universidade de Santiago de Compostela

Centro de Investigación Biomédica en Red

Instituto de Investigación Sanitaria de Santiago

Instituto de Salud Carlos III

Center for Research in Molecular Medicine and Chronic Diseases

Helmholtz Zentrum München

German Center for Diabetes Research

Deutsches Diabetes-Zentrum e.V.

Heinrich Heine University Düsseldorf

Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition

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CPT1A in AgRP neurons is required for sex-dependent regulation of feeding and thirst

Biology of Sex Differences (2023)

Sebastián Zagmutt Paula Mera Ismael González‐García Kevin Ibeas María del Mar Romero

Fatty acid metabolism in the hypothalamus has an important role in food intake, but its specific role in AgRP neurons is poorly understood. Here, we examined whether carnitinea palmitoyltransferase 1A (CPT1A), a key enzyme in mitochondrial fatty acid oxidation, affects energy balance.

Human physiology

10.1186/s13293-023-00498-8

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Citations (7)

Pharmacological Inhibition of PI3K Reduces Adiposity and Metabolic Syndrome in Obese Mice and Rhesus Monkeys

Cell Metabolism (2015)

Ana Ortega-Molina Elena Lopez-Guadamillas Julie A. Mattison Sarah J. Mitchell Maribel Muñoz‐Martín

Steatosis

Diet-induced obese

10.1016/j.cmet.2015.02.017

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Citations (90)

Hypothalamic Astrocytes as a Specialized and Responsive Cell Population in Obesity

International Journal of Molecular Sciences (2021)

Ismael González‐García Cristina García‐Cáceres

Astrocytes are a type of glial cell anatomically and functionally integrated into the neuronal regulatory circuits for the neuroendocrine control of metabolism. Being functional integral compounds of synapses, astrocytes are actively involved in the physiological regulatory aspects of metabolic control, but also in the pathological processes that link neuronal dysfunction and obesity. Between brain areas, the hypothalamus harbors specialized functional circuits that seem selectively vulnerable to metabolic damage, undergoing early cellular rearrangements which are thought to be at the core of the pathogenesis of diet-induced obesity. Such changes in the hypothalamic brain region consist of a rise in proinflammatory cytokines, the presence of a reactive phenotype in astrocytes and microglia, alterations in the cytoarchitecture and synaptology of hypothalamic circuits, and angiogenesis, a phenomenon that cannot be found elsewhere in the brain. Increasing evidence points to the direct involvement of hypothalamic astrocytes in such early metabolic disturbances, thus moving the study of these glial cells to the forefront of obesity research. Here we provide a comprehensive review of the most relevant findings of molecular and pathophysiological mechanisms by which hypothalamic astrocytes might be involved in the pathogenesis of obesity.

Proinflammatory cytokine

Pathogenesis

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Neuroglia

10.3390/ijms22126176

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Citations (29)

Ceramides in the central control of metabolism

Trends in Endocrinology and Metabolism (2024)

Miguel López Carlos Diéguez Manuel Tena‐Sempere Ismael González‐García

10.1016/j.tem.2024.06.007

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Small extracellular vesicle-mediated targeting of hypothalamic AMPKα1 corrects obesity through BAT activation

Nature Metabolism (2021)

Edward Milbank Nathalia Romanelli Vicente Dragano Ismael González‐García Marcos Ríos García Verónica Rivas-Limeres

AMP-Activated Protein Kinase

10.1038/s42255-021-00467-8

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Citations (63)

Astrocytic GABA in LHA is an obesity ‘thermostat’

Nature Metabolism (2023)

Ismael González‐García Cristina García‐Cáceres

10.1038/s42255-023-00849-0

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Divide et impera: How mitochondrial fission in astrocytes rules obesity

Molecular Metabolism (2021)

Ismael González‐García Ophélia Le Thuc Martin Jastroch Cristina García‐Cáceres

10.1016/j.molmet.2020.101159

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Citations (3)

Ovarian insufficiency impairs glucose-stimulated insulin secretion through activation of hypothalamic de novo ceramide synthesis

Metabolism (2021)

Kelly Meneyrol Ánxela Estévez‐Salguero Ismael González‐García Jeanne Guitton Mohammed Taouis

Energy homeostasis

Homeostasis

Blood sugar regulation

10.1016/j.metabol.2021.154846

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Citations (6)

Olanzapine depot exposure in male rats: Dose-dependent lipogenic effects without concomitant weight gain

European Neuropsychopharmacology (2015)

Johan Fernø Kari M. Ersland I.H. Duus Ismael González‐García Kjell Ove Fossan

Dopamine antagonist

10.1016/j.euroneuro.2015.03.002

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Citations (38)

Lack of Ovarian Secretions Reverts the Anabolic Action of Olanzapine in Female Rats

The International Journal of Neuropsychopharmacology (2017)

Silje Skrede Ismael González‐García Luís Martins Rolf K. Berge Rubén Nogueiras

Olanzapine is an orexigenic antipsychotic drug associated with serious metabolic adverse effects in humans. Development of valid rodent models for antipsychotic-induced metabolic adverse effects is hampered by the fact that such effects occur in females only. Estradiol is a predominant female hormone that regulates energy balance. We hypothesized that the female-specific hyperphagia and weight gain induced by olanzapine in the rat are dependent on the presence of estrogens.Female sham-operated or ovariectomized rats were treated with a single injection of olanzapine depot formulation. Food intake, body weight, plasma lipids, lipogenic gene expression, energy expenditure, and thermogenic markers including brown adipose tissue uncoupling protein 1 protein levels were measured. Olanzapine was also administered to ovariectomized rats receiving estradiol replacement via the subcutaneous (peripheral) or intracerebroventricular route.Orexigenic effects of olanzapine were lost in ovariectomized female rats. Ovariectomized rats treated with olanzapine had less pronounced weight gain than expected from their food intake. Accordingly, brown adipose tissue temperature and protein levels of uncoupling protein 1 were elevated. Replacement in ovariectomized rats with either peripherally or centrally administered estradiol reduced food intake and body weight. Cotreatment with olanzapine blocked the anorexigenic effect of peripheral, but not central estradiol.Our results indicate that the ovarian hormone estradiol plays an important role in olanzapine-induced hyperphagia in female rats and pinpoint the complex effects of olanzapine on the balance between energy intake and thermogenesis.

Orexigenic

10.1093/ijnp/pyx073

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Citations (18)