hyperphagia/hypoxia

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Gestational hypoxia disrupts the neonatal leptin surge and programs hyperphagia and obesity in male offspring in the Sprague-Dawley rat.

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The effect of gestational hypoxia on the neonatal leptin surge, development of hypothalamic arcuate nuclei (ARH) projections and appetite that could contribute to the programming of offspring obesity is lacking. We examined the effect of 12% O2 from gestational days 15-19 in the Sprague-Dawley rat

Hypoxia-inducible factor directs POMC gene to mediate hypothalamic glucose sensing and energy balance regulation.

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Hypoxia-inducible factor (HIF) is a nuclear transcription factor that responds to environmental and pathological hypoxia to induce metabolic adaptation, vascular growth, and cell survival. Here we found that HIF subunits and HIF2α in particular were normally expressed in the mediobasal hypothalamus

Endothelial HIF-1α Enables Hypothalamic Glucose Uptake to Drive POMC Neurons.

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Glucose is the primary driver of hypothalamic proopiomelanocortin (POMC) neurons. We show that endothelial hypoxia-inducible factor 1α (HIF-1α) controls glucose uptake in the hypothalamus and that it is upregulated in conditions of undernourishment, during which POMC neuronal activity is decreased.

Assessment of sleep and breathing in adults with prader-willi syndrome: a case control series.

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OBJECTIVE Prader-Willi syndrome (PWS) is a genetic disorder (linked to chromosome 15q11-13) characterized by hypotonia and developmental delay, hyperphagia and obesity, hypersomnia and abnormal sleep, and behavioral problems. Such patients may also be at increased risk of obstructive sleep apnea

[Effects of hypocaloric diet on respiratory manifestations in Willi-Prader syndrome].

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BACKGROUND Prader-Willi syndrome (PWS) is a multisystem disorder with hyperphagia and obesity. Breathing disorders such as snoring, sleep apnea syndrome, and sleep hypoventilation have also been reported. METHODS Jonathan was born with the typical features of PWS. He developed exercise dyspnea,

Periodic apnea, exercise hypoventilation, and hypothalamic dysfunction.

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Periodic apnea and exercise hypoventilation were observed in a 14-year-old boy. Hyperphagia, obesity, serum hyperosmolality without diabetes insipidus or appropriate thirst, and retardation of growth and sexual development indicated a hypothalamic disorder. Neurologic evaluation was normal except

Drug-induced activation of the nervous control of inflammation: a novel possibility for the treatment of hypoxic damage.

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Together with undernutrition and, on the opposite, overeating and obesity, sudden tissue hypoperfusion is the most important cause of mortality and disability worldwide. Tissue hypoperfusion/hypoxia rapidly triggers an unrestrained inflammatory cascade that is the main responsible for the severity

Morbid obesity in an adolescent with Prader-Willi syndrome.

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Prader-Willi syndrome is an uncommon multisystem genetic disorder caused by defects of chromosome 15 (15qll-ql3), often due to deletions or uniparental disomy The syndrome is characterized by neonatal hypotonia, dysmorphic facial features, short stature, motor and mental disabilities, behavioral

[The effects of clomipramine on diurnal sleepiness and respiratory parameters in a a case of Prader-Willi syndrome].

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The association of Prader-Willi-syndrome with breathing disturbances such as sleep apnea syndrome and/or hypoxemia during REM sleep, REM sleep abnormalities and excessive daytime sleepiness is well known. We report the case of an 11-year-old boy who presented with Prader-Willi syndrome, obesity

Metabolic phenotype and adipose and liver features in a high-fat Western diet-induced mouse model of obesity-linked NAFLD.

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nonalcoholic fatty liver disease (NAFLD), an obesity and insulin resistance associated clinical condition - ranges from simple steatosis to nonalcoholic steatohepatitis. To model the human condition, a high-fat Western diet that includes liquid sugar consumption has been used in mice. Even though

Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes.

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Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact

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