Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indications of rethoracotomy after esophagectomy for esophageal cancer are reviewed in this paper. Hemothorax, pneumothorax, pyothorax and chylothorax are the main causes of rethoracotomy. Complications indicating rethoracotomy are summarized as follows: 1) Hemothorax; emergency rethoracotomy is indicated in cases of bleeding through the chest drain over 100ml/hr, which is continuing over 5 hours or in cases when normal blood pressure cannot be maintained without blood transfusion. In many cases the bleeding point is the chest wall, from the branches of the intercostal artery. 2) Pneumothorax; reoperation for pneumothorax is rare. But rethoracotomy and bullectomy or closure of fustula is indicated when a large volume of air leakage and lung collapse continues over a week. 3) Pyothorax; old pyothorax with bronchial fistula is treated by closure of fistula and plombage with omentum or muscle flap. 4) Chylothorax; chylothorax is not a frequent complication of esophageal surgery but when it occurs reoperation is not rare. In cases with 1,500ml/day or more of chyle drainage for over 5 days under fasting with intravenous hyperalimentation, rethoracotomy and ligation of thoracic duct is indicated.
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PMID:[Indications of rethoracotomy after esophagectomy for esophageal cancer]. 877 13

In common forms of obesity, hyperphagia, hyperinsulinemia, and hyperleptinemia coexist. Here, we demonstrate rapid induction of insulin and leptin resistance by short-term overfeeding. After 3 and 7 days on the assigned diet regimen, rats were tested for their biological responses to acute elevations in plasma insulin and leptin concentrations. Severe resistance to the metabolic effects of both leptin and insulin ensued after just 3 days of overfeeding. During the insulin clamp studies, glucose production was decreased by approximately 70% in control rats and 28-53% in overfed rats. Similarly, leptin infusion doubled the contribution of gluconeogenesis to glucose output in control rats but failed to modify gluconeogenesis in overfed animals. These findings demonstrate a paradoxical and rapid collapse of the leptin system in response to nutrient excess. This partial failure is tightly coupled with the onset of insulin resistance.
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PMID:Overfeeding rapidly induces leptin and insulin resistance. 1172 62

Neuropeptide Y (NPY) is involved in the central regulation of appetite, sexual behavior, and reproductive function. We have previously shown that chronic infusion of NPY into the lateral ventricle of normal rats produced an obesity syndrome characterized by hyperphagia, hyperinsulinism and collapse of reproductive function. We further demonstrated that acute inhibition of LH secretion in castrated rats was preferentially mediated by the NPY receptor subtype 5 (Y(5)). In the present study, the effects of chronic, central infusion of NPY, or the mixed Y2-Y5 agonist PYY(3-36), were evaluated both in normal male C57BL/6J mice and Sprague-Dawley rats. After a 7-day infusion to male mice, both NPY and PYY(3-36) at 5 nmol per day, induced marked hyperphagia leading to significant increases in body and fat pad weights. Furthermore, both compounds markedly reduced several markers of the reproductive axis. In the rat study, PYY(3-36) was more active than NPY to inhibit the pituitary-testicular axis, confirming the importance of the Y5 subtype for such effects. In the mouse, chronic NPY infusion induced a sustained increase in corticosterone and insulin secretion. Plasma leptin levels were also markedly increased possibly explaining the observed reduction in gene expression for hypothalamic NPY. Gene expression for hypothalamic POMC was reduced in the NPY- or PYY(3-36)-infused mice, suggesting that NPY exacerbated food intake by both acting through its own receptor(s), and reducing the satiety signal driven by the POMC-derived alpha-MSH. The present study in the mouse suggests in analogy with available rat data, that constant exposure to elevated NPY in the hypothalamic area unabatedly enhances food intake leading to an obesity syndrome including increased adiposity, insulin resistance, hypercorticism, and hypogonadism, reminiscent of the phenotype of the ob/ob mouse, that displays elevated hypothalamic NPY secondary to lack of leptin negative feedback action.
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PMID:Chronic administration of neuropeptide Y into the lateral ventricle of C57BL/6J male mice produces an obesity syndrome including hyperphagia, hyperleptinemia, insulin resistance, and hypogonadism. 1173 9