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Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

http://www.wikidata.org/entity/Q36741980

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From observation to experimentation: leptin action in the mediobasal hypothalamus Do all roads lead to Rome? The role of neuro-immune interactions before birth in the programming of offspring obesity Developmental programming of hypothalamic neuronal circuits: impact on energy balance control Uncovering novel roles of nonneuronal cells in body weight homeostasis and obesity Substantial and robust changes in microRNA transcriptome support postnatal development of the hypothalamus in rat.Modeling Diet-Induced Obesity with Obesity-Prone Rats: Implications for Studies in Females Over-expression of leptin receptors in hypothalamic POMC neurons increases susceptibility to diet-induced obesity Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring Hypothalamic neuroendocrine circuitry is programmed by maternal obesity: interaction with postnatal nutritional environment.Critical determinants of hypothalamic appetitive neuropeptide development and expression: species considerations.Brain-endocrine interactions: a microvascular route in the mediobasal hypothalamus.Gamma-protocadherins regulate the functional integrity of hypothalamic feeding circuitry in mice.PTP1B and SHP2 in POMC neurons reciprocally regulate energy balance in mice.Inducible neuronal inactivation of Sim1 in adult mice causes hyperphagic obesity.Changes in melanocortin expression and inflammatory pathways in fetal offspring of nonhuman primates fed a high-fat diet Early overnutrition results in early-onset arcuate leptin resistance and increased sensitivity to high-fat diet.Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding.Perinatal environment and its influences on metabolic programming of offspring.Interaction of perinatal and pre-pubertal factors with genetic predisposition in the development of neural pathways involved in the regulation of energy homeostasis Developmental gene x environment interactions affecting systems regulating energy homeostasis and obesity.Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity.Large litter rearing enhances leptin sensitivity and protects selectively bred diet-induced obese rats from becoming obese.Metabolic imprinting, programming and epigenetics - a review of present priorities and future opportunities.Sexual dimorphism in offspring glucose-sensitive hypothalamic gene expression and physiological responses to maternal high-fat diet feeding.Anti-obesity sodium tungstate treatment triggers axonal and glial plasticity in hypothalamic feeding centers.Effect of diet on preference and intake of sucrose in obese prone and resistant rats.Protein-tyrosine phosphatase 1B (PTP1B) is a novel regulator of central brain-derived neurotrophic factor and tropomyosin receptor kinase B (TrkB) signaling Effects of reduced weight maintenance and leptin repletion on functional connectivity of the hypothalamus in obese humans.Methyl donor supplementation blocks the adverse effects of maternal high fat diet on offspring physiology.Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity Neonatal overnutrition causes early alterations in the central response to peripheral ghrelin.Neonatal ghrelin programs development of hypothalamic feeding circuits.Effects of chronic weight perturbation on energy homeostasis and brain structure in mice Ghrelin-induced adiposity is independent of orexigenic effects Metabolic programming in the immediate postnatal life.Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring.Amylin-induced central IL-6 production enhances ventromedial hypothalamic leptin signaling.Orphanin FQ in the mediobasal hypothalamus facilitates sexual receptivity through the deactivation of medial preoptic nucleus mu-opioid receptors.Transient early food restriction leads to hypothalamic changes in the long-lived crowded litter female mice.Role of VMH ketone bodies in adjusting caloric intake to increased dietary fat content in DIO and DR rats.

P2860

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P2860

Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

http://www.wikidata.org/entity/Q36741980

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2008 nî lūn-bûn

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2008年论文

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2008年论文

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name

Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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prefLabel

Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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J.CMET.2007.12.001

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Cell Metabolism

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Hypothalamic neural projections are permanently disrupted in diet-induced obese rats

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P2093

Barry E Levin

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Christa M Patterson

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Judith N Gorski

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Richard B Simerly

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Stephen Chen

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P2860

Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

Altered hypothalamic leptin, insulin, and melanocortin binding associated with moderate-fat diet and predisposition to obesity

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

Formation of projection pathways from the arcuate nucleus of the hypothalamus to hypothalamic regions implicated in the neural control of feeding behavior in mice.

Trophic action of leptin on hypothalamic neurons that regulate feeding.

Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.

Identifying hypothalamic pathways controlling food intake, body weight, and glucose homeostasis.

Programming of appetite and type 2 diabetes.

Perinatal nutrition and hormone-dependent programming of food intake.

Developmental programming of hypothalamic feeding circuits.

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179-185

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2

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7

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Sebastien G Bouret

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2442478

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