A calorie-rich diet is one reason for the continuous spread of metabolic syndromes in western societies. Smart food design is one powerful tool to prevent metabolic stress, and the search for suitable bioactive additives is a continuous task. The nutrient-sensing insulin pathway is an evolutionary conserved mechanism that plays an important role in metabolism, growth and development. Recently, lipid cues capable to stimulate insulin signaling were identified. However, the mechanistic base of their activity remains obscure to date. We show that specific Akt/Protein-kinase B isoforms are responsive to different calorie-rich diets, and potentiate the activity of the cellular insulin cascade. Our data add a new dimension to existing models and position Drosophila as a powerful tool to study the relation between dietary lipid cues and the insulin-induced cellular signal pathway.
The computation of reliable, chemically correct atom maps from educt/product pairs has turned out to be a difficult problem in cheminformatics because the chemically correct solution is not necessarily an optimal solution for combinatorial formulations such as maximum common subgraph problems. As a consequence, competing models have been devised and compared in extensive benchmarking studies. Due to isomorphisms among products and educts it is not immediately obvious, however, when two atom maps for a given educt/product pairs are the same. We formalize here the equivalence of atom maps and show that equivalence of atom maps is in turn equivalent to the isomorphism of labeled auxiliary graphs. In particular, we demonstrate that Fujita's Imaginary Transition State can be used for this purpose. Numerical experiments show that practical feasibility. Generalizations to the equivalence of subgraph matches, double pushout graph transformation rules, and mechanisms of multi-step reactions are discussed briefly.
A calorie-rich diet is one reason for the continuous spread of metabolic syndromes in western societies. Smart food design is one powerful tool to prevent metabolic stress, and the search for suitable bioactive additives is a continuous task. The nutrient-sensing insulin signaling pathway is an evolutionary conserved mechanism that plays an important role in metabolism, growth and development. Recently, lipid cues capable to stimulate insulin signaling were identified. However, the mechanistic base of their activity remains obscure to date. Here, we show that specific AKT/ Protein kinase B isoforms are responsive to dietary lipid extract compositions and potentiate cellular insulin signaling levels. Our data add a new dimension to existing models and position Drosophila as a powerful model to study the relation between dietary lipid cues and the insulin induced cellular signal cascade.
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