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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Feeding Behavior

 
 
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Disease relevance of Feeding Behavior

 

Psychiatry related information on Feeding Behavior

 

High impact information on Feeding Behavior

  • A new framework for understanding the control of feeding behavior, with special emphasis on the evolution of hunger, the initiation of feeding, and its dependence on patterns of blood glucose, is the subject of this review [10].
  • Urocortin-deficient mice have normal basal feeding behavior and stress responses, but show heightened anxiety-like behaviors in the elevated plus maze and open-field tests [11].
  • Transgenic expression of syndecan-1 uncovers a physiological control of feeding behavior by syndecan-3 [12].
  • When administered centrally to rats, these peptides stimulate food consumption. prepro-orexin mRNA level is up-regulated upon fasting, suggesting a physiological role for the peptides as mediators in the central feedback mechanism that regulates feeding behavior [13].
  • Thus, isoforms of a putative neuropeptide receptor generate natural variation in C. elegans feeding behavior [14].
 

Chemical compound and disease context of Feeding Behavior

  • Experiments with four types of invertebrates showed that feeding behavior and dietary uptake control bioaccumulation of cadmium, silver, nickel, and zinc [15].
  • These results are in agreement with recent reports of the anatomical and biochemical effects of intracerebral kainic acid injections and suggest that the observed effect on feeding behavior is related to the destruction of neurons in the lateral hypothalamus [16].
  • Insulin and corticosterone, which are known to affect hypothalamic NPY and CRH expression, were not different between these two groups, making it unlikely that they can account for the differences in either feeding behavior or hypothalamic peptide expression [17].
  • To further explore the role of CCK in humans, the effect on satiety and eating behavior of a specific CCK-receptor antagonist, loxiglumide, that preferentially inhibits peripheral (CCK-A) receptors was investigated [18].
  • This receptor subfamily, which is believed to be the target of the anti-migraine drug sumatriptan and may regulate feeding behavior, anxiety, depression, cardiac function and movement, can now be approached on a molecular level [19].
 

Biological context of Feeding Behavior

  • These results indicate that NMU plays an important role in the regulation of feeding behavior and energy metabolism independent of the leptin signaling pathway [20].
  • Leptin, injected intraperitoneally (i.p.) at low doses (4-120 microg/kg), which did not influence feeding behavior for the first 3 hr postinjection, decreased food intake dose dependently by 47-83% during the first hour when coinjected with a subthreshold dose of CCK [21].
  • Upon reduction of the litter size, some mutants survive into adulthood and display growth retardation with no apparent brain or behavioral abnormalities, suggesting that Hap1 function is essential only for early postnatal feeding behavior [22].
  • It is proposed that these rhythms, involving a predark rise in CORT and NPY gene expression leading to a peak in CORT and peptide levels at dark onset, are active in stimulating feeding behavior, particularly carbohydrate ingestion, which predominates at that time [23].
  • These results suggest that calcium/calmodulin-dependent protein kinase II induced phosphorylation of CREB may be involved in regulating feeding behavior induced by NPY [24].
 

Anatomical context of Feeding Behavior

 

Gene context of Feeding Behavior

  • These are the first two variants associated with the pathophysiology of ED in different populations and support a role for BDNF in the susceptibility to aberrant eating behaviors [30].
  • Recently, it has been shown that targeted disruption of Hap1 in mice results in early postnatal death as a result of depressed feeding behavior [22].
  • Identification of a novel hypothalamic neuropeptide Y receptor associated with feeding behavior [31].
  • To determine the physiological importance of GLP-1 receptor (GLP-1R)-leptin interactions, we studied islet function and feeding behavior in ob/ob:GLP-1R(-/-) mice [32].
  • Agouti-related protein (AGRP) is an endogenous antagonist of melanocortin action that functions in the hypothalamic control of feeding behavior [33].
 

Analytical, diagnostic and therapeutic context of Feeding Behavior

References

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  3. IMPACT, a protein preferentially expressed in the mouse brain, binds GCN1 and inhibits GCN2 activation. Pereira, C.M., Sattlegger, E., Jiang, H.Y., Longo, B.M., Jaqueta, C.B., Hinnebusch, A.G., Wek, R.C., Mello, L.E., Castilho, B.A. J. Biol. Chem. (2005) [Pubmed]
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  11. Urocortin-deficient mice show hearing impairment and increased anxiety-like behavior. Vetter, D.E., Li, C., Zhao, L., Contarino, A., Liberman, M.C., Smith, G.W., Marchuk, Y., Koob, G.F., Heinemann, S.F., Vale, W., Lee, K.F. Nat. Genet. (2002) [Pubmed]
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  15. Influences of dietary uptake and reactive sulfides on metal bioavailability from aquatic sediments. Lee, B.G., Griscom, S.B., Lee, J.S., Choi, H.J., Koh, C.H., Luoma, S.N., Fisher, N.S. Science (2000) [Pubmed]
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  18. Role of circulating cholecystokinin in control of fat-induced inhibition of food intake in humans. Drewe, J., Gadient, A., Rovati, L.C., Beglinger, C. Gastroenterology (1992) [Pubmed]
  19. A subfamily of 5-HT1D receptor genes. Hartig, P.R., Branchek, T.A., Weinshank, R.L. Trends Pharmacol. Sci. (1992) [Pubmed]
  20. Neuromedin U has a novel anorexigenic effect independent of the leptin signaling pathway. Hanada, R., Teranishi, H., Pearson, J.T., Kurokawa, M., Hosoda, H., Fukushima, N., Fukue, Y., Serino, R., Fujihara, H., Ueta, Y., Ikawa, M., Okabe, M., Murakami, N., Shirai, M., Yoshimatsu, H., Kangawa, K., Kojima, M. Nat. Med. (2004) [Pubmed]
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  22. Huntingtin-associated protein 1 (Hap1) mutant mice bypassing the early postnatal lethality are neuroanatomically normal and fertile but display growth retardation. Dragatsis, I., Zeitlin, S., Dietrich, P. Hum. Mol. Genet. (2004) [Pubmed]
  23. Hypothalamic neuropeptide Y and its gene expression: relation to light/dark cycle and circulating corticosterone. Akabayashi, A., Levin, N., Paez, X., Alexander, J.T., Leibowitz, S.F. Mol. Cell. Neurosci. (1994) [Pubmed]
  24. Neuropeptide Y treatment and food deprivation increase cyclic AMP response element-binding in rat hypothalamus. Sheriff, S., Chance, W.T., Fischer, J.E., Balasubramaniam, A. Mol. Pharmacol. (1997) [Pubmed]
  25. Altered cerebrospinal fluid neuropeptide Y and peptide YY immunoreactivity in anorexia and bulimia nervosa. Kaye, W.H., Berrettini, W., Gwirtsman, H., George, D.T. Arch. Gen. Psychiatry (1990) [Pubmed]
  26. GABA in the nucleus accumbens shell participates in the central regulation of feeding behavior. Stratford, T.R., Kelley, A.E. J. Neurosci. (1997) [Pubmed]
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