By Prof. Antonio Vidal-Puig MD, PhD, FRCP (auth.), Matej Orešič, Antonio Vidal-Puig (eds.)
The target of this publication is to supply the objective viewers, in particular scholars of medication, Biology, structures Biology and Bioinformatics, in addition to skilled researchers in examine fields proper to metabolic syndrome (MetS) with an summary of the demanding situations and possibilities in platforms biology and the way it may be used to take on MetS. specifically, the goals are: (1) to supply an creation to the foremost organic methods concerned about the pathophysiology of MetS; (2) by using particular examples, offer an advent to the newest applied sciences that use a structures biology method of learn MetS; and (3) to offer an summary of the mathematical modeling methods for learning MetS.
The sincerely written chapters through prime specialists within the box offers distinct descriptions an important for the original place of this booklet and its concentrate on the applying of structures biology to take on particular pathophysiologically suitable points of MetS and gives a important sensible advisor to this learn community.
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Extra info for A Systems Biology Approach to Study Metabolic Syndrome
ChREBP plays a key role in the conversion of carbohydrates to TGs in response to glucose excess (Fig. 1) (Towle et al. 1997). ChREBP is activated directly from glucose, and 3 The Liver in Metabolic Syndrome 35 indirectly from insulin through the induction of glucokinase which allows the conversion of phosphorylated glucose to xylulose-5-phosphate, with subsequent activation of protein phosphatase 2A (PP2A) that dephosphorylates and activates ChREBP (Kabashima et al. 2003). ChREBP is inhibited by phosphorylation that is mediated by PKA and AMPK (Kawaguchi et al.
This is a good example of allostatic adaptation (the concept introduced in Chap. 1) aimed at induction of short-term corrective changes to regulatory systems. However, when such an adaptive response remains activated for long periods of time, the maintenance of metabolic homeostasis might actually come at a metabolic cost, or ‘collateral damage’, defined by McEwen as allostatic load (Korte et al. 2005). In the case of SREBP1c knock-down, the allostatic load is for example the accumulation of cholesterol due to the adaptive activation of SREBP2.
The common denominator is the presence of macrovescicular hepatic steatosis, resulting from accumulation of triglycerides (TGs) within hepatocytes, in the absence of significant alcohol intake. If steatosis is a normal feature in the liver of migratory birds, that need to store energy in order to face long periods of fasting, this condition is not a physiological finding in humans (Capeau 2008). As a consequence, NAFLD is not a benign condition with a non-progressive course, as initially believed, but a progressive condition leading to NASH, and finally to fibrosis, cryptogenic cirrhosis, and increased risk for 3 The Liver in Metabolic Syndrome 29 hepatocellular carcinoma (Bugianesi 2005; Caldwell et al.