Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Juvenile neuronal ceroid lipofuscinosis or Batten disease (JNCL) is a neurodegenerative disorder characterized by blindness, seizures, cognitive decline and early death. Brain atrophy and retinitis pigmentosa ensue because of neuronal and photoreceptor apoptosis. The CLN3 gene defective in JNCL encodes a novel 438 amino acid protein. Most affected genes harbor a deletion resulting in a truncated protein. CLN3 overexpression in NT2 cells enhances growth, reverses growth inhibition induced by serum starvation and protects from apoptosis induced by vincristine, staurosporine, and etoposide but not from death caused by ceramide. CLN3 modulates endogenous and vincristine-activated ceramide, and therefore suppresses apoptosis by impacting generation of ceramide.
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PMID:CLN3 defines a novel antiapoptotic pathway operative in neurodegeneration and mediated by ceramide. 1019 Nov 18

Neuroanatomical and functional studies in the eating disorders (ED) are reviewed. Typically, anorexia nervosa (AN) is associated with cerebral spinal fluid spaces enlargement which generally recover as a function of re-feeding. However, specific cortical areas fail to correct in weight restored anorectic patients suggesting trait-related abnormalities. Functional changes in AN associated with starvation reverse with weight recovery, however, reduced 5-HT2A receptor binding may be fundamental to the pathophysiology of AN since this remains after long term weight restoration. Structural studies of bulimia nervosa (BN) provide evidence of brain atrophy, in the absence of significant weight loss but potentially related to chronic dietary restriction. Functional investigations reveal reduced thalamic and hypothalamic serotonin transporter availability in BN which increases with longer illness duration. Thus, BN is associated with substantial structural and functional alterations despite normal weight. Recent advances in neuroimaging techniques and their interpretation are increasing our understanding of normal processes in the control of food intake including neuroanatomical correlates of hunger and satiety. Taken together with the structural and functional changes observed in the ED, neuroimaging provides a powerful platform to identify the underlying trait-related pathophysiological mechanisms in the aetiology and maintenance of AN and BN.
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PMID:Neuroimaging in eating disorders. 1474 36

Anorexia nervosa (AN) commonly arises during adolescence, leading to interruptions of somatic and psychological development as well as to cortical atrophy and reductions of brain volume. While most brain changes shift towards normal with weight restoration, it is not certain whether they are related to the loss of brain cells, neuropil or merely due to fluid shifts. We measured S100B serum concentrations and psychometric characteristics in 34 patients with acute AN, 19 weight-recovered patients and 35 healthy control women (HCW). Plasma tryptophan and leptin levels were determined as markers for malnutrition and neuroendocrine adaptation to semi-starvation. Peripheral S100B concentrations of acute and former AN patients were not elevated and not statistically different from HCW. BMI, peripheral leptin levels and measures of psychopathology as well as executive cognitive functioning did not correlate with S100B. Plasma tryptophan was positively related to S100B. Our results are in line with our previous findings showing unaltered GFAP and NSE plasma levels in patients with acute AN. Together they do not support hypotheses comprising the degeneration of glial or neuronal cells to explain common signs of brain atrophy in patients with acute AN.
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PMID:S100B in underweight and weight-recovered patients with anorexia nervosa. 1842 88