A Systems Biology Approach to Study Metabolic Syndrome by Prof. Antonio Vidal-Puig MD, PhD, FRCP (auth.), Matej

By Prof. Antonio Vidal-Puig MD, PhD, FRCP (auth.), Matej Orešič, Antonio Vidal-Puig (eds.)

The target of this e-book is to supply the objective viewers, particularly scholars of medication, Biology, structures Biology and Bioinformatics, in addition to skilled researchers in examine fields appropriate to metabolic syndrome (MetS) with an summary of the demanding situations and possibilities in structures biology and the way it may be used to take on MetS. specifically, the goals are: (1) to supply an advent to the most important organic techniques excited about the pathophysiology of MetS; (2) by utilizing particular examples, supply an creation to the newest applied sciences that use a platforms biology method of learn MetS; and (3) to provide an summary of the mathematical modeling methods for learning MetS.

The sincerely written chapters by way of major specialists within the box offers specified descriptions an important for the original place of this booklet and its specialise in the appliance of platforms biology to take on particular pathophysiologically suitable features of MetS and offers a necessary useful consultant to this learn community.

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Extra info for A Systems Biology Approach to Study Metabolic Syndrome

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Small changes in enzyme concentrations and fluxes through their pathways may produce large changes in the 2 Systems Biology in Human Health and Disease 21 Fig. 3 Factors influencing the metabolome and proteome and the key analytical platforms for systems biology to study health and disease. The metabolome is sensitive to genetic and environmental factors which may together contribute to the disease. Metabolomics is thus a powerful phenotyping platform in biomedical studies concentrations of metabolites which are the end products of these pathways (Kell 2006).

1995; Shulman and Mangelsdorf 2005). NRs show considerable specificity in their activation and tissue-specific expression (Bookout et al. 2006), and they can work as monomers, homodimers, and heterodimers (Mangelsdorf et al. 1995) . In the human genome 48 NRs have been identified, while in rodents there are 49 (Mangelsdorf et al. 1995). NRs are characterized by a conserved modular structure including a ligandindependent activation function domain (AF-1), a ligand-binding domain (LBD), a DNA-binding domain (DBD, binding to a specific hormone response element), and a region involved in the transcriptional activation of target-gene expression (Lanz et al.

2008). The mechanism responsible for the inadequate increase in hepatic TG export is unknown, but it might be related to inability of the liver to secrete large VLDL particles, which cannot be secreted through the sinusoidal endothelial pores (Horton et al. 1999). In fact, secretion rate of VLDL-ApoB-100 is equal between subjects with high and low intrahepatic TGs content, with consequent production of very large TG-rich VLDL. Moreover, the hepatic synthesis of ApoB-100, which represents the rate-limiting step in the formation of VLDL, has been shown markedly altered by insulin (Dashti et al.

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