hyperphagia/necrose

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Near-total gastric necrosis caused by acute gastric dilatation.

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Gastric dilatation caused by psychogenic polyphagia or bulimia may, under extreme circumstances, progress to total gastric necrosis. We have described a patient in whom acute abdominal symptoms and signs developed while he was receiving psychiatric treatment. Laparotomy showed massive gastric

Magnetic resonance imaging of feline hippocampal necrosis.

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The clinical, neuropathologic, and magnetic resonance (MR) imaging features in four cats with necrosis of the hippocampus and piriform lobe are described. All cats had acute generalized seizures and behavioral changes including aggression, salivation, polyphagia, and disorientation. Routine

Hyperphagia contributes to the normal body composition and protein-energy balance in HIV-infected asymptomatic men.

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Wasting can occur at an early stage of HIV infection. Both reduced energy intake and increased resting energy expenditure (REE) have been considered as factors in wasting with predominant lean body mass loss, suggesting disturbances of protein metabolism. Our aim was to study protein-energy

Gastrojejunostomy for pyloric stenosis after acute gastric dilatation due to overeating.

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A 34-year-old woman presented at our hospital with abdominal distention due to overeating. Acute gastric dilatation was diagnosed. The patient was hospitalized, and nasogastric decompression was initiated. On hospitalization day 3, she developed shock, and her respiratory state deteriorated,

[Gastric necrosis from acute dilatation without underlying psychiatric disorder].

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Acute gastric dilatation with necrosis is a rare and severe complication associated with anorexia nervosa, bulimia, and psychogenic polyphagia. The Authors report an unusual case without underlying psychiatric context. Gastric necrosis was suspected based on imaging findings (plain radiograph and

Systemic phlorizin prevents gold thioglucose necrosis in the ventromedial hypothalamus.

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Intraventricular and intrahypothalamic infusions of phlorizin (PHL) are known to cause hyperphagia and to prevent gold thioglucose (GTG) lesion formation in the ventromedial hypothalamus (VMH), respectively. In this study, PHL, administered IP in a large dose (900 mg/kg), completely inhibited GTG

Upregulation of uncoupling protein 2 mRNA in genetic obesity: lack of an essential role for leptin, hyperphagia, increased tissue lipid content, and TNF-alpha.

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Uncoupling protein 2 (UCP2) has been proposed to play a prominent role in the regulation of energy balance. UCP2 mRNA expression is upregulated in white adipose tissue (WAT) and liver, but is not altered in skeletal muscle in genetically obese ob/ob mice. The mechanisms involved in the upregulation

IL-10 gene transfer upregulates arcuate POMC and ameliorates hyperphagia, obesity and diabetes by substituting for leptin.

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BACKGROUND Obesity and metabolic syndrome are the major risk factors for cardiovascular disease. Obesity is caused by increased food intake and/or decreased energy expenditure. Leptin potently inhibits food intake and promotes energy expenditure. These effects of leptin involve the activation of

Gastric rupture and necrosis in Prader-Willi syndrome.

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Hyperphagia and obesity are common features in individuals with Prader-Willi syndrome (PWS). Demographic and cause-of-death data from individuals with PWS were obtained through a national support organization. Four reports of unexpected mortality due to gastric rupture and necrosis were found in 152

Gangliocytoma of third ventricle: hyperphagia, somnolence, and dementia.

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A 55-year-old man had hydrocephalus caused by a third-ventricular tumor. Mentation improved after ventricular shunting and radiation therapy. Progressive hyperphagia, obesity, memory impairment, and hypersomnolence developed 13 months later, and he died 2 years after diagnosis. At necropsy, a

Activation of nuclear factor kappa B pathway and reduction of hypothalamic oxytocin following hypothalamic lesions.

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BACKGROUND Hypothalamic obesity (HO) occurs in patients with tumors and lesions in the medial hypothalamic region. In this study, a hyperphagic rat model of combined medial hypothalamic lesions (CMHL) was used to test which specific inflammatory molecules are involved. METHODS In order to target

Physiologic and endocrinologic characterization of male sex-biased diabetes in C57BLKS/J mice congenic for the fat mutation at the carboxypeptidease E locus.

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The fat gene in mice represents a recessive mutation at the carboxypeptidase E (Cpe) locus. The mutant allele (Cpe(fat)) encodes a highly unstable enzyme and produces an obesity phenotype characterized by attenuated processing of prohormones such as proinsulin that require this exopeptidase for full

Gastric Dilatation and Abdominal Compartment Syndrome in a Child with Prader-Willi Syndrome.

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BACKGROUND Prader-Willi syndrome (PWS) is a genetic disorder characterized by initial muscular hypotonia and feeding difficulties, and later an insatiable appetite, hyperphagia and obesity along with mild to moderate intellectual impairment. Affected individuals' food-seeking behavior and suspected

Excitotoxic lesions of the paraventricular hypothalamus: metabolic and cardiac effects.

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The excitotoxin, N-methyl-D-aspartic acid (NMDA), was used to lesion cell bodies, but not fibers-of-passage, in the paraventricular hypothalamus. Bilateral injections of NMDA (12.6 nmol/100 nl) were made into the paraventricular hypothalamus in halothane-anesthetized male Sprague-Dawley rats. Water

Idiopathic segmental infarction of the greater omentum successfully treated by laparoscopy: report of case.

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Idiopathic or spontaneous segmental infarction of the greater omentum (ISIGO) is a rare cause of acute right-sided abdominal pain. The symptoms simulate acute appendicitis in 66% of cases and cholecystitis in 22%. Progressive peritonitis usually dictates laparotomy, and an accurate diagnosis is

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