Persönlicher Status und Werkzeuge

Sprachwahl

Nutritional Systems Biology

What is Nutritional Systems Biology?

My definition: Mammalian metabolism is the expression of a continuum of adaptational changes to a rapidly (in time and quantity) changing supply of energy, macro- and micronutrients and non-nutritional components of foods. Nutritional systems biology could be defined as the approach to understand the key processes that regulate metabolism at all levels of complexity, to simulate it and to predict the outcome of any alteration of the system. Nutritional systems biology (NSB) starts at the molecular and cellular levels and takes the regulatory processes onto the level of the interorgan flow of information and metabolites to describe most comprehensively the organismic response and the processes quantitatively in mathematical terms.

So, NSB ist the approach to defining how a genome scopes with its nutritional environment and this is taken onto the level of modelling and predicting the metabolic, physiological or pathophysiological outcome of any alteration in nutrition.

To be able to take NSB to life, we need to start with the genetic information available, employ profiling techniques at the mRNA, protein and metabolite levels and phenotype the organisms response by all means of physiological methods available. From there models are generated using sohisticated software tools, new hypothesis are generated and those are tested and revised based on new experiments. In the end, it is the goal to describe like in an electronic circuit the underlying changes in the biological system that determine the phenotypic outcome. 

 

In our approaches to Nutritional Systems Biology we assess the responses of cells in culture or of our model organisms (transgenic C. elegans lines or genetically modified mice) by performing profiling at the mRNA, protein and metabolite levels with the goal of understanding the wiring of underlying the changes and how these are linked to the phenotypic alterations.

The example shown in the figure are the metabolic pathways identified as altered (including changes in mRNA levels, protein levels and metabilite levels) in renal cells in our mouse line that lacks the tubular peptide transporter PEPT2. By the seroquel info site applied we could identify alterations in renal cell redox- and glutathione status that helped us to define a challenge experiment that finally proved that these alterations can lead to a pathophysiological state.

last updated: 11.10.08