Despite the current epidemic of obesity and metabolic syndrome, how metabolism regulates food intake is not clear. Rodents, after being fully fed, stop eating and often go to sleep. This is defined as the behavioral sequence of satiety. We found that C. elegans mimics the same behavioral sequence of satiety; after full feeding, worms stop eating and become quiescent as if sleeping. We found that insulin, TGF b and cGMP signals acting through PKG (cGMP-dependent protein kinase) are necessary to regulate quiescence induced by satiety [1]. During fasting, worms use their stored fat [2]. The fat lost in 12 hours of fasting is fully recovered after 3 hours of refeeding (personal observation, You YJ). To investigate if fat storage and metabolism regulate quiescence, we modified fat storage and examined changes in quiescence. To examine the effect of increased fat storage in quiescence, we fed worms oleic acid, a monounsaturated fatty acid [3]. To examine the effect of reduced fat storage, we tested several mutants that fail to store fat. Adding oleic acid enhances quiescence in wild type, suggesting that fat storage can change quiescence behavior. A fat-6; fat-7 double mutant stores less triglyceride than wild type (personal communication, Watt J.) and show reduced quiescence. The defect of fat-6; fat-7 in quiescence could be rescued by adding oleic acid during refeeding. Furthermore, RNAi of sbp-1, a worm homolog of SREBP-1c which is necessary for worms to store fat [4], also reduced quiescence. To further investigate the roles of metabolism in quiescence, we performed an RNAi screen with 163 metabolic genes identified by Wang et. al. [5]. So far we have found 11 candidate genes most of which are involved in fat metabolism, suggesting that proper fat storage is necessary for worms to show intact quiescence. This work was supported by research grant DK074065 from the National Institutes of Health. Reference 1.You, Y.J., et al., Insulin, cGMP, and TGF-beta signals regulate food intake and quiescence in C. elegans: a model for satiety. Cell Metab, 2008. 7(3): p. 249-57. 2.McKay, R.M., et al., C elegans: a model for exploring the genetics of fat storage. Dev Cell, 2003. 4(1): p. 131-42. 3.Brock, T.J., J. Browse, and J.L. Watts, Genetic regulation of unsaturated fatty acid composition in C. elegans. PLoS Genet, 2006. 2(7): p. e108. 4.Yang, F., et al., An ARC/Mediator subunit required for SREBP control of cholesterol and lipid homeostasis. Nature, 2006. 442(7103): p. 700-4. 5.Wang, M.C., E.J. O''Rourke, and G. Ruvkun, Fat metabolism links germline stem cells and longevity in C. elegans. Science, 2008. 322(5903): p. 957-60.