Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity. - Wikidata - awgldk - TriplyDB

Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity.

Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity.

http://www.wikidata.org/entity/Q34093323

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Regulation of Estrogen Receptor α Expression in the Hypothalamus by Sex Steroids: Implication in the Regulation of Energy Homeostasis Plasticity of the Melanocortin System: Determinants and Possible Consequences on Food Intake Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention Age-Associated Weight Gain, Leptin, and SIRT1: A Possible Role for Hypothalamic SIRT1 in the Prevention of Weight Gain and Aging through Modulation of Leptin Sensitivity Brain-gut-adipose-tissue communication pathways at a glance Role of non-neuronal cells in body weight and appetite control Neuroinflammatory basis of metabolic syndrome Brain regulation of energy balance and body weight.Uncovering novel roles of nonneuronal cells in body weight homeostasis and obesity Neuroinflammation in overnutrition-induced diseases Estrogen, astrocytes and the neuroendocrine control of metabolism Obesity-driven synaptic remodeling affects endocannabinoid control of orexinergic neurons Brain Control of Plasma Cholesterol Involves Polysialic Acid Molecules in the Hypothalamus.Regional astrogliosis in the mouse hypothalamus in response to obesity.Communication breakdown: the impact of ageing on synapse structure.Hypothalamic gliosis associated with high-fat diet feeding is reversible in mice: a combined immunohistochemical and magnetic resonance imaging study.Obesity induces neuroinflammation mediated by altered expression of the renin-angiotensin system in mouse forebrain nuclei.Mitochondrial dynamics controlled by mitofusins regulate Agrp neuronal activity and diet-induced obesity.Obesity- and aging-induced excess of central transforming growth factor-β potentiates diabetic development via an RNA stress response Leptin regulates glutamate and glucose transporters in hypothalamic astrocytes.Maternal deprivation exacerbates the response to a high fat diet in a sexually dimorphic manner.Exercise, energy intake, glucose homeostasis, and the brain Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity Hypothalamic microinflammation: a common basis of metabolic syndrome and aging.Sixteen years and counting: an update on leptin in energy balance Evidence for a novel functional role of astrocytes in the acute homeostatic response to high-fat diet intake in mice Effects of chronic weight perturbation on energy homeostasis and brain structure in mice High fat diet intake during pre and periadolescence impairs learning of a conditioned place preference in adulthood.Glucose effectiveness in obese children: relation to degree of obesity and dysglycemia.Reduction of high-fat diet-induced obesity after chronic administration of brain-derived neurotrophic factor in the hypothalamic ventromedial nucleus Brain innate immunity regulates hypothalamic arcuate neuronal activity and feeding behavior.Axon-like basal processes in enteroendocrine cells: characteristics and potential targets Obesity is associated with hypothalamic injury in rodents and humans.Neuroendocrine-autonomic integration in the paraventricular nucleus: novel roles for dendritically released neuropeptides.Developmental changes in synaptic distribution in arcuate nucleus neurons Elevated hypothalamic TCPTP in obesity contributes to cellular leptin resistance.Proopiomelanocortin, agouti-related protein, and leptin in human cerebrospinal fluid: correlations with body weight and adiposity.Peroxisome proliferation-associated control of reactive oxygen species sets melanocortin tone and feeding in diet-induced obesity Withaferin A is a leptin sensitizer with strong antidiabetic properties in mice.Hypothalamic inflammation and gliosis in obesity

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P2860

Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity.

http://www.wikidata.org/entity/Q34093323

description

2010 nî lūn-bûn

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2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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

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Synaptic input organization of ...... c reactive gliosis and obesity

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Barry E Levin

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Beatrix Sarman

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Erzsebet Borok

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Hella S Brönneke

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Marya Shanabrough

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Matthias H Tschöp

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Pablo J Enriori

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Paul T Pfluger

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Peter Sotonyi

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Sabrina Diano

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P2860

Positional cloning of the mouse obese gene and its human homologue

Ghrelin controls hippocampal spine synapse density and memory performance

Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite

Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene

Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus

Topographic mapping of VMH --> arcuate nucleus microcircuits and their reorganization by fasting.

Hypothalamic and pituitary c-Jun N-terminal kinase 1 signaling coordinately regulates glucose metabolism.

Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons.

Trophic action of leptin on hypothalamic neurons that regulate feeding.

Decreased cerebrospinal-fluid/serum leptin ratio in obesity: a possible mechanism for leptin resistance.

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107

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Cristina García-Cáceres

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Diego Perez-Tilve

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