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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Cell Dev. Biol. | doi: 10.3389/fcell.2019.00206

Selective phosphorylation of Akt/Protein-kinase B isoforms in response to dietary cues

 Laura C. Trautenberg1,  Elodie Prince1, Cornelia Maas1, Freya Honold1,  Michal Grzybek2, 3* and  Marko Brankatschk1*
  • 1BIOTEC, Technische Universität Dresden, Germany
  • 2Deutsche Zentrum für Diabetesforschung (DZD), Germany
  • 3Paul Langerhans Institute Dresden, German Center for Diabetes Research, Dresden University of Technology, Germany

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 signalling 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.

Keywords: Drosophila, Sacharomyces cerevisae, Yeast lipids, AKT isoform, Akt phoshphorylation, high caloric diet, insulin signaling, PKB, Akt, Cystobasidium oligophagum, Microbe-host interaction, Axenic, yeast growth phase , Akt Ser505, Akt Thr342

Received: 26 Apr 2019; Accepted: 06 Sep 2019.

Copyright: © 2019 Trautenberg, Prince, Maas, Honold, Grzybek and Brankatschk. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Dr. Michal Grzybek, Deutsche Zentrum für Diabetesforschung (DZD), Oberschleissheim, 85764, Germany,
Dr. Marko Brankatschk, BIOTEC, Technische Universität Dresden, Dresden, 01307, Lower Saxony, Germany,