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)

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

The world is currently experiencing an obesity epidemic as declared by the World Health Organization. The traditional view is that behaviour leading to overeating and under-activity is the major contributing factor for this worldwide epidemic. However, several microbes are linked to obesity in animals and humans. On the one hand, various microbes, including animal and human viruses, bacteria, parasites and scrapie agents, increase adiposity in several animal models. Some of these microbes show an association with human obesity, but conclusive evidence for a causative role of microbes in human obesity is lacking. On the other hand, obese individuals show an altered response to infections. Obesity is often associated with impaired immune function, which may lead to increased susceptibility to infection with a number of different pathogens. Hence, certain microbes appear to induce obesity, whereas, obesity itself may exacerbate certain other infections. Linking the two phenomenon is the immunological property of adipocytes and their progenitors. For instance, proliferating pre-adipocytes share embryonic origin with immune cells and exhibit phagocytic activity. Taken together it appears that there is a close interrelationship between adipose tissue, inflammatory response, immune system and infections. Hence, it is conceivable that in response to certain infections, adipose tissue expands similar to the expansion of cells of the immune system. The impaired immune function of adipose tissue in obesity may exacerbate infections. Considering the global obesity epidemic, it is necessary to further investigate both phenomena.
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PMID:Microbes and obesity--interrelationship between infection, adipose tissue and the immune system. 2350 25