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)

Chronic wasting disease (CWD), a prion disease of North American deer, elk and moose, affects both free-ranging and captive cervids. The potential host range for CWD remains uncertain. The susceptibility of the ferret to CWD was examined experimentally by administering infectious brain material by the intracerebral (IC) or oral (PO) route. Between 15 and 20 months after IC inoculation, ferrets developed neurological signs consistent with prion disease, including polyphagia, somnolence, piloerection, lordosis and ataxia. Upon first sub-passage of ferret-adapted CWD, the incubation period decreased to 5 months. Spongiform change in the neuropil was most marked in the basal ganglia, thalamus, midbrain and pons. The deposition of PrP(CWD) was granular and was occasionally closely associated with, or localized within, neurons. There were no plaque-like or perivascular PrP aggregates as seen in CWD-infected cervids. In western blots, the PrP(CWD) glycoform profile resembled that of CWD in deer, typified by a dominant diglycosylated glycoform. CWD disease in ferrets followed IC but not PO inoculation, even after 31 months of observation. These findings indicate that CWD-infected ferrets share microscopical and biochemical features of CWD in cervids, but appear to be relatively resistant to oral infection by primary CWD inoculum of deer origin.
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PMID:Experimental chronic wasting disease (CWD) in the ferret. 1838 26

Prion diseases are fatal neurodegenerative diseases that can induce endocrinopathies. The basis of altered endocrine function in prion diseases is not well understood, and the purpose of this study was to investigate the spatiotemporal relationship between energy homeostasis and prion infection in hamsters inoculated with either the 139H strain of scrapie agent, which induces preclinical weight gain, or the HY strain of transmissible mink encephalopathy (TME), which induces clinical weight loss. Temporal changes in body weight, feed, and water intake were measured as well as both non-fasted and fasted concentrations of serum glucose, insulin, glucagon, beta-ketones, and leptin. In 139H scrapie-infected hamsters, polydipsia, hyperphagia, non-fasted hyperinsulinemia with hyperglycemia, and fasted hyperleptinemia were found at preclinical stages and are consistent with an anabolic syndrome that has similarities to type II diabetes mellitus and/or metabolic syndrome X. In HY TME-infected hamsters, hypodipsia, hypersecretion of glucagon (in both non-fasted and fasted states), increased fasted beta-ketones, fasted hypoglycemia, and suppressed non-fasted leptin concentrations were found while feed intake was normal. These findings suggest a severe catabolic syndrome in HY TME infection mediated by chronic increases in glucagon secretion. In both models, alterations of pancreatic endocrine function were not associated with PrP(Sc) deposition in the pancreas. The results indicate that prominent endocrinopathy underlies alterations in body weight, pancreatic endocrine function, and intake of food. The prion-induced alterations of energy homeostasis in 139H scrapie- or HY TME-infected hamsters could occur within areas of the hypothalamus that control food satiety and/or within autonomic centers that provide neural outflow to the pancreas.
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PMID:Prominent pancreatic endocrinopathy and altered control of food intake disrupt energy homeostasis in prion diseases. 1843 55