Abstract：
:Despite the prevalence of obesity and its related diseases, the signaling pathways for appetite control and satiety are not clearly understood. Here we report C. elegans quiescence behavior, a cessation of food intake and movement that is possibly a result of satiety. C. elegans quiescence shares several characteristics of satiety in mammals. It is induced by high-quality food, it requires nutritional signals from the intestine, and it depends on prior feeding history: fasting enhances quiescence after refeeding. During refeeding after fasting, quiescence is evoked, causing gradual inhibition of food intake and movement, mimicking the behavioral sequence of satiety in mammals. Based on these similarities, we propose that quiescence results from satiety. This hypothesized satiety-induced quiescence is regulated by peptide signals such as insulin and TGF-beta. The EGL-4 cGMP-dependent protein kinase functions downstream of insulin and TGF-beta in sensory neurons including ASI to control quiescence in response to food intake.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
You YJ,Kim J,Raizen DM,Avery Ldoi
10.1016/j.cmet.2008.01.005subject
Has Abstractpub_date
2008-03-01 00:00:00pages
249-57issue
3eissn
1550-4131issn
1932-7420pii
S1550-4131(08)00006-5journal_volume
7pub_type
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