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Thursday, June 26, 2008

Systems Properties Of Insulin Signaling Revealed

A team of Swedish researchers has characterized the properties of new signalling systems human insulin in fat cells. Their mathematical modelling provides a better understanding of energy level maintenance (through the hormone insulin) within our bodies.

Entravé function of insulin is the cardinal cause of type 2 diabetes, which currently affects nearly 250 million people worldwide. The disease causes a metabolic malfunction due to incorrect information transfer of insulin concentration in the blood inside the cells of liquid (the cytosol). This transfer of information is through a complex network of protein-protein interactions. The skeleton of the network was characterized, but the systems details, including the relative importance and the time scales of interactions, were hitherto unknown.

Because of the complexity of the network, it has proved difficult to reach such an understanding through simple systems experimental techniques and reasoning. Hence, the team collected experimentally time series data on human fat cells in vitro and evaluated various explanations by translating mechanistic explanations corresponding mathematical models.

In this study, modeling indicated that the recycling of receptors or between the membrane and the cytosol, or reactions of proteins activated lowest in the network are involved in the transfer of information during the first minutes after insulin stimulation.

As more detailed data are available, the authors predict that mathematical modelling will become an increasingly important tool for data analysis, and to promote understanding of insulin and cellular signalling.


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Journal reference:

Citation: Cedersund G, J Roll, Ulfhielm E, Danielsson A, Tidefelt H, et al. Model-Based Testing Assumption of the main mechanisms in the initial phase of Insulin Signaling. Comput Biol, 4 (6): e1000096. DOI: 10.1371/journal.pcbi.1000096
Adapted from material supplied by the Public Library of Science, via EurekAlert! A service of AAAS.

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