Identification of Sphingolipid Metabolites That Induce Obesity via Misregulation of Appetite, Caloric Intake and Fat Storage in Drosophila
Figure 9
Sphingolipid regulation of caloric intake and fat mobilization.
Both saturated and unsaturated fats act as precursor “input” molecules in the production of “output” sphingolipid intermediates, specifically ceramide and S1P, which act to transduce a physiological response. (Left) Sphingolipid metabolism regulates Akh cell viability and function (Right). After a meal, S1P accumulates downstream of elevated ceramide. S1P, either directly or indirectly (through dRYamide), induces dNepY receptor signaling in the hindgut, inducing appetite suppression, reduced caloric intake and downregulation of dNepYr mRNA expression (negative feedback).