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Trautenberg, L. C.

Publications and source records attributed to Trautenberg, L. C..

3 recordsLinked to original sources

Insulin regulates systemic lipid traffic in starving animals

In periods of malnutrition starving organisms initiate the reorganization and degradation of cellular lipids. Yet, the build-up of lipid stores is reported in animals entering early starvation stages. Anabolic lipid metabolism is regulated by many circuits including the insulin/insulin- like growth factor signaling (IIS) cascade. The regulative role of IIS ligands in food deprived animals is often neglected, since supporting evidence for this notion is largely missing. Here we show that in starving adult Drosophila melanogaster IIS is required to stabilize the transport of circulating lipids and sugars, and is essential for the initial increase of lipid stores in fat body cells. Further, we demonstrate that the Drosophila insulin-like peptides (dIlp) 2 and 5 regulate the cellular IIS cascade differentially. To its end we speculate that each hormone initiates complementary measures that increase the starvation resistance of adult flies.

physiology↗

Diet and heat - one neuronal subset two responses

The Insulin signal cascade is one of the best studied metabolic circuits, and shows a remarkable high molecular and functional conservation across the animal kingdom. Insulin-producing cells respond directly to nutritional cues in circulation and receive modulatory input from connected neuronal networks. Neuronal control is rapid and integrates a wide range of variables including dietary change or environmental temperature. However, despite various detailed studies that demonstrated the potential of neuronal regulation the physiological relevance of this circuit remains elusive. In Drosophila, Insulin-like peptide 7 (dIlp7)-producing neurons are wired with Insulin-producing cells. We found a dual role for this neuronal subset: a.) activated dilp7-producing neurons are required to facilitate development at high temperatures, and if confronted with calorie-rich food that represses neuronal activity b.) their product, dIlp7, regulates Insulin signalling levels. Our work shows that Insulin-producing cells not simply integrate signals from circulating nutritional cues and neuronal inputs, but switch to neuronal control in response to dietary composition.

physiology↗

Selective phosphorylation of AKT isoforms in response to dietary cues

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.

physiology↗