Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We examined gene expression of corticotropin-releasing hormone and neuropeptide Y level in the hypothalamic paraventricular nucleus of mouse bearing a human oral squamous cell carcinoma. A cell line derived from a human oral squamous cell carcinoma was inoculated into the lower dorsal area of nude mice. Body weight, tumor size and daily food intake were recorded every morning. Mice were sacrificed for corticotropin-releasing hormone mRNA in situ hybridization and neuropeptide Y immunohistochemistry, when the tumor ratio reached to 11-13% of real body weight. The results were compared with the age-matching non-tumor controls injected with saline instead of carcinoma cell. Body weight gain was significantly reduced in tumor bearing mice, however, no compensatory hyperphagia was found, i.e. daily food intake of the tumor mice did not differ from the non-tumor mice. Both neuropeptide Y immunoreactivity and corticotropin-releasing hormone mRNA level were significantly increased in the hypothalamic paraventricular nucleus of tumor mice. These results suggest that a human oral squamous cell carcinoma may induce anorexia, at least partly, via increasing the hypothalamic expression of corticotropin-releasing hormone in the tumor subjects. Additionally, neuropeptide Y-induced feeding appears to be inhibited in this tumor anorexia model, and this may correlate with increased expression of corticotropin-releasing hormone.
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PMID:Neuropeptide Y immunoreactivity and corticotropin-releasing hormone mRNA level are increased in the hypothalamus of mouse bearing a human oral squamous cell carcinoma. 1556 70

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.
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PMID:Canine hyperadrenocorticism. 1603 96

A patient with type 2 diabetes and hypothalamic damage due to a suprasellar tumor developed impaired glycemic control and central obesity. The patient showed exaggerated adrenocorticotropic hormone responsiveness as determined by a corticotrophin releasing hormone test and elevated serum leptin concentrations associated with ravenous appetite and insulin resistance mediated in part through disturbances in leptin signaling. Combination treatment with metformin and pioglitazone was markedly effective in improving glycemic control. Additionally, metformin treatment showed marked anorectic effects on the hyperphagia. This case has important implications for the pathogenesis and management of diabetes in patients with hypothalamic-pituitary-adrenal axis deficiencies.
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PMID:Markedly improved glycemic control and enhanced insulin sensitivity in a patient with type 2 diabetes complicated by a suprasellar tumor treated with pioglitazone and metformin. 1615 82

Endocrine diseases in the dog commonly manifest with dermatological lesions. Hypothyroidism is the most common endocrinopathy and usually presents with alopecia in areas of wear, seborrhea, and recurrent infections. Common clinical signs associated with hyperadrenocorticism include polyuria, polydipsia, and polyphagia. The most common dermatological manifestation of hyperadrenocorticism is bilaterally symmetrical alopecia sparing the head and distal extremities. Pyoderma is a common finding associated with immunosuppression. Less commonly, calcinosus cutis may occur. Sex hormone excess, primarily hyperestrogenism and hyperandrogenism, may also be associated with dermatological signs. Usually, dogs are intact, and the excess production is due to testicular or ovarian neoplasia.
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PMID:Comparative dermatology--canine endocrine dermatoses. 1682 13

Stimulation of tumour growth by intensive exogenous nutrient administration could be a major clinical problem when nutritional support is provided in malnourished cancer patients. Nutritional repletion has been clearly shown to stimulate tumour growth in animal models but not in humans. The purpose of this prospective study was to evaluate the effect of pre-operative nutritional support on the proliferative characteristics of gastric tumour cells evaluated by 3H-thymidine (3HT) incorporation and flow cytometry (FCM). Thirty-three malnourished patients with advanced gastric cancer were allocated randomly into two groups receiving different types of nutritional support during the interval between endoscopy and operation: parenteral and/or enteral hyperalimentation (Group 1), and oral alimentation as possible or peripheral fluids (Group 2). In 16 patients with diploid tumours the percentage of 3HT labelled cells and of cells in S+G(2)M phase did not differ between the multiple samples taken from the mucosal surface of the neoplasia. Tumour samples showed higher mean values of cycling cells than the surrounding normal tissue. Both methods (3HT - FCM) demonstrate that tumour cell proliferation is not enhanced following a prolonged period of pre-operative artificial nutrition.
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PMID:Pre-operative nutritional support and tumour cell kinetics in malnourished patients with gastric cancer. 1683 61

Obesity is typically associated with increased tumor susceptibility, whereas caloric restriction, a regimen resulting in leanness, inhibits carcinogenesis. The link between adiposity and malignancies suggests that adipose tissue may influence carcinogenesis. An adipose tissue hormone, leptin, could be procarcinogenic because it stimulates proliferation in various tissues and tumor cell lines. Leptin may contribute to the correlation between adiposity and malignancies as its levels are usually increased in obese subjects and reduced by caloric restriction. We hypothesized that leptin deficiency, despite obesity, would inhibit carcinogenesis in leptin-null ob/ob mice and tested this hypothesis in two models: (a) two-stage skin carcinogenesis initiated by 7,12-dimethylbenz(a)anthracene and promoted by phorbol 12-myristate 13-acetate (PMA) and (b) p53 deficiency. Contrary to a typical association between obesity and enhanced carcinogenesis, obese ob/ob mice developed induced skin papillomas and spontaneous p53-deficient malignancies, mostly lymphomas, similarly to their lean littermates. Surprisingly, lipodystrophic (ZIP) mice that had very little both adipose tissue and leptin were highly susceptible to carcinogenesis. Hyperphagia, hyperinsulinemia, and hyperglycemia are unlikely to have contributed significantly to the enhancement of carcinogenesis in ZIP mice because similarly hyperphagic, hyperinsulinemic, and hyperglycemic ob/ob mice had normal susceptibility to carcinogenesis. Our data suggest that, in contrast to a well-known correlation between obesity and cancer, the direct effect of adipose tissue may rather be protective.
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PMID:Susceptibility to induced and spontaneous carcinogenesis is increased in fatless A-ZIP/F-1 but not in obese ob/ob mice. 1695 Dec 7

Cachexia is a clinical wasting syndrome that occurs in multiple disease states, and is associated with anorexia and a progressive loss of body fat and lean mass. The development of new therapeutics for this disorder is needed due to poor efficacy and multiple side effects of current therapies. The pivotal role played by the central melanocortin system in regulating body weight has made this an attractive target for novel cachexia therapies. The mixed melanocortin receptor antagonist AgRP is an endogenous peptide that induces hyperphagia. Here, we used AgRP(83-132) to investigate the ability of melanocortin antagonism to protect against clinical features of cachexia in two distinct animal models. In an acute model, food intake and body weight gain were reduced in mice exposed to radiation (300 RAD), and delivery of AgRP(83-132) into the lateral cerebral ventricle prevented these effects. In a chronic tumor cachexia model, adult mice were injected subcutaneously with a cell line derived from murine colon-26 adenocarcinoma. Typical of cachexia, tumor-bearing mice progressively reduced body weight and food intake, and gained significantly less muscle mass than controls. Administration of AgRP(83-132) into the lateral ventricles significantly increased body weight and food intake, and changes in muscle mass were similar to the tumor-free control mice. These findings support the idea that antagonism of the central melanocortin system can reduce the negative impact of cachexia and radiation therapy.
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PMID:Central infusion of the melanocortin receptor antagonist agouti-related peptide (AgRP(83-132)) prevents cachexia-related symptoms induced by radiation and colon-26 tumors in mice. 1720 51

Hypothalamic injury from acquired structural damage due to infiltrative disease, tumor, or their treatment aftereffects frequently results in the development of an obesity syndrome characterized by a rapid, unrelenting weight gain that may be accompanied by severe hyperphagia. Weight gain occurs from the disruption of the normal homeostatic functioning of the hypothalamic centers responsible for controlling satiety and hunger and regulating energy balance with resulting hyperphagia, autonomic imbalance, reduction of energy expenditure, and hyperinsulinemia. Curtailment of weight increase has traditionally been refractory to usual dietary and lifestyle interventions. Pharmacotherapy targeting insulin secretion and augmenting sympathetic output have been attempted to promote weight loss or attenuate weight gain. In addition, case reports suggest that bariatric surgery may be an effective treatment option for these patients. Hormonal deficits are often present, and their management may also have consequences for weight control. Hypothalamic obesity confers significant morbidity and mortality, and there is a need for greater elucidation of its risk factors and pathogenesis so that more effective interventions can be developed.
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PMID:Review of physiology, clinical manifestations, and management of hypothalamic obesity in humans. 1832 43

The mammalian target of rapamycin (mTOR) promotes anabolic cellular processes in response to growth factors and metabolic cues. The TSC1 and TSC2 tumor suppressors are major upstream inhibitory regulators of mTOR signaling. Mice with Rip2/Cre-mediated deletion of Tsc1 (Rip-Tsc1cKO mice) developed hyperphagia and obesity, suggesting that hypothalamic disruption (for which Rip2/Cre is well known) of Tsc1 may dysregulate feeding circuits via mTOR activation. Indeed, Rip-Tsc1cKO mice displayed increased mTOR signaling and enlarged neuron cell size in a number of hypothalamic populations, including Pomc neurons. Furthermore, Tsc1 deletion with Pomc/Cre (Pomc-Tsc1cKO mice) resulted in dysregulation of Pomc neurons and hyperphagic obesity. Treatment with the mTOR inhibitor, rapamycin, ameliorated the hyperphagia, obesity, and the altered Pomc neuronal morphology in developing or adult Pomc-Tsc1cKO mice, and cessation of treatment reinstated these phenotypes. Thus, ongoing mTOR activation in Pomc neurons blocks the catabolic function of these neurons to promote nutrient intake and increased adiposity.
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PMID:Critical role for hypothalamic mTOR activity in energy balance. 1935 17

The present case is 74 years old man who was hospitalized to treat lung tumor suspected of malignancy. Because the superior vena cava thrombus was also revealed by radiological examination, he was performed lobectomy and thrombectomy at the same time. He has past history of intravenous hyperalimentation for 15 days, and we supposed the event to be the cause of the thrombus. Venous thrombus has developed again in the left subclavian vein in spite of the anticoagulant therapy at the early postoperative period. The level of serum factor XII turned out to be low by the precise examination, of which possible contribution to thrombus formation was suspected.
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PMID:[Superior vena cava thrombosis in a case with low serum factor XII]. 2224 91


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