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)

A 13-year-old warmblood mare was presented because of progressive weight loss, general weakness and trembling. On examination the horse stood with its head lowered and the limbs placed under the body. On lifting its head spasms of the neck muscles could be observed. At the same time the horse developed trembling over the lower neck and muscle fasciculations continued over the whole body. Additional signs included frequent recumbency, polyphagia and facial hyperaesthesia. The horse showed no signs of ataxia. Haematology was normal. Blood biochemistry revealed slight increased aspartate aminotransferase (AST: 1060 U/I) and creatine kinase levels (CK: 441 U/I). Based on the clinical findings equine motor neuron disease was diagnosed. The horse was euthanatized due to poor prognosis and the progression of symptoms. The typical neurodegenerative changes found on histological examination of the spinal cord confirmed the diagnosis.
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PMID:[Equine motor neuron disease (EMND). A case report]. 928 83

Ciliary Neurotrophic Factor (CNTF) was first characterized as a trophic factor for motor neurons in the ciliary ganglion and spinal cord, leading to its evaluation in humans suffering from motor neuron disease. In these trials, CNTF caused unexpected and substantial weight loss, raising concerns that it might produce cachectic-like effects. Countering this possibility was the suggestion that CNTF was working via a leptin-like mechanism to cause weight loss, based on the findings that CNTF acts via receptors that are not only related to leptin receptors, but also similarly distributed within hypothalamic nuclei involved in feeding. However, although CNTF mimics the ability of leptin to cause fat loss in mice that are obese because of genetic deficiency of leptin (ob/ob mice), CNTF is also effective in diet-induced obesity models that are more representative of human obesity, and which are resistant to leptin. This discordance again raised the possibility that CNTF might be acting via nonleptin pathways, perhaps more analogous to those activated by cachectic cytokines. Arguing strongly against this possibility, we now show that CNTF can activate hypothalamic leptin-like pathways in diet-induced obesity models unresponsive to leptin, that CNTF improves prediabetic parameters in these models, and that CNTF acts very differently than the prototypical cachectic cytokine, IL-1. Further analyses of hypothalamic signaling reveals that CNTF can suppress food intake without triggering hunger signals or associated stress responses that are otherwise associated with food deprivation; thus, unlike forced dieting, cessation of CNTF treatment does not result in binge overeating and immediate rebound weight gain.
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PMID:Ciliary neurotrophic factor activates leptin-like pathways and reduces body fat, without cachexia or rebound weight gain, even in leptin-resistant obesity. 1129 75

We wished to determine whether patients with amyotrophic lateral sclerosis (ALS) show behavioural changes similar to those of frontotemporal dementia (FTD). There is accumulating evidence to suggest a link between ALS and FTD, yet there has been little systematic exploration of behaviour in ALS. An informant based semi-structured behavioural interview, sensitive to the behavioural changes of FTD, was administered to carers of 16 consecutive patients attending a motor neuron disease clinic. Findings varied across the group. At one extreme informants reported no behavioural change, whereas at the other they reported a spectrum of behaviours similar to those seen in FTD. Changes in affect and social behaviour were most common, although some patients also showed altered response to sensory stimuli, gluttony and indiscriminate eating, behavioural stereotypies and compulsions. Behavioural changes were mirrored by SPECT abnormalities in the frontal and/or temporal lobes. Thus, behavioural changes of the type seen in FTD may be present even in a small consecutive cohort of ALS patients. Detection of behavioural change is crucial for optimal management.
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PMID:Behaviour in amyotrophic lateral sclerosis. 1842 98