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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trained, unanaesthetised dogs with jejunal fistula and adapted to 2 h meal-time showed transient taste-correlated changes in pressure (mm H2O) but not in frequency of intestinal motility. Intestinal pressure was increased on bitter taste both before meal-time (4.7 +/- 0.2 mm) and after it (13.1 +/- 0.9 mm) over respective basal pressure (before meal 3.2 +/- 0.4 mm), after meal 10.6 +/- 1.4 mm), whereas it was decreased on sweetness of saccharin (before meal 1.1 +/- 0.1 mm, after meal 4.8 +/- 0.5 mm), and glucose (before meal 1.7 +/- 0.2 mm; after meal 8.8 +/- 0.9 mm). Taste-induced motility changes were more pronounced on starvation than on fed state.
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PMID:Gustatory effects on intestinal motility of dogs. 366 90

Drosophila is a powerful model in which to study the molecular and cellular basis of taste coding. Flies sense tastants via populations of taste neurons that are activated by compounds of distinct categories. The past few years have borne witness to studies that define the properties of taste neurons, identifying functionally distinct classes of sweet and bitter taste neurons that express unique subsets of gustatory receptor (Gr) genes, as well as water, salt, and pheromone sensing neurons that express members of the pickpocket (ppk) or ionotropic receptor (Ir) families. There has also been significant progress in terms of understanding how tastant information is processed and conveyed to higher brain centers, and modulated by prior dietary experience or starvation.
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PMID:Molecular neurobiology of Drosophila taste. 2610 53

Nutrient deprivation can lead to dramatic changes in feeding behavior, including acceptance of foods that are normally rejected. In flies, this behavioral shift depends in part on reciprocal sensitization and desensitization of sweet and bitter taste, respectively. However, the mechanisms for bitter taste modulation remain unclear. Here, we identify a set of octopaminergic/tyraminergic neurons, named OA-VLs, that directly modulate bitter sensory neuron output in response to starvation. OA-VLs are in close proximity to bitter sensory neuron axon terminals and show reduced tonic firing following starvation. We find that octopamine and tyramine potentiate bitter sensory neuron responses, suggesting that starvation-induced reduction in OA-VL activity depotentiates bitter taste. Consistent with this model, artificial silencing of OA-VL activity induces a starvation-like reduction in bitter sensory neuron output. These results demonstrate that OA-VLs mediate a critical step in starvation-dependent bitter taste modulation, allowing flies to dynamically balance the risks associated with bitter food consumption against the threat of severe starvation.
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PMID:Starvation-Induced Depotentiation of Bitter Taste in Drosophila. 2772 Jun 24