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

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

ISBN-10: 3319010077

ISBN-13: 9783319010076

ISBN-10: 3319010085

ISBN-13: 9783319010083

The objective of this e-book is to supply the objective viewers, in particular scholars of drugs, Biology, structures Biology and Bioinformatics, in addition to skilled researchers in learn fields suitable 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 approaches keen on the pathophysiology of MetS; (2) by utilizing particular examples, supply an advent to the most recent applied sciences that use a platforms biology method of research MetS; and (3) to offer an outline of the mathematical modeling methods for learning MetS.

The truly written chapters by means of prime specialists within the box offers distinctive descriptions the most important for the original place of this e-book and its concentrate on the appliance of platforms biology to take on particular pathophysiologically appropriate points of MetS and offers a worthy useful advisor to this learn community.

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Extra info for A Systems Biology Approach to Study Metabolic Syndrome

Example text

However, although FAO appears to be increased in liver of both NAFLD and NASH patients (Sanyal et al. 2001), this increase is not sufficient per se to prevent TG accumulation. Overall, contrasting results have been reported about FAO in NAFLD, so further studies are needed (Higuchi et al. 2008). Mitochondrial dysfunction results in increased production of reactive oxygen species (ROS) and, thus, oxidative stress. ROS can activates stress responses leading to increased activity of mitogen activate protein kinase (MAPK) and c-Jun N-terminal kinase (JNK), two kinases that inhibit IRS1 and IRS2, with consequent decreased activation of PI3K.

As mentioned before FAs can be both esterified to TGs or oxidized with the production of adenosine triphosphate (ATP). The uptake of FA into the mitochondria matrix is regulated by CPT-1 and -2. CPT-1 levels have been found decreased in patients with NAFLD, consequentially to the inhibition by high levels of malonyl-CoA, suggesting a reduction in mitochondrial FAO (Nakamuta et al. 2005a). However, although FAO appears to be increased in liver of both NAFLD and NASH patients (Sanyal et al. 2001), this increase is not sufficient per se to prevent TG accumulation.

In patients with NAFLD, VLDL synthesis and export are impaired. In a state of IR the rates of VLDL secretion are increased and accelerated, with subsequent enhancement of serum levels of LDL and of atherogenic small LDL (sLDL). The delipidation chain is under the control of two enzymes; cholesteryl ester transfer protein (CETP), and hepatic lipase (HL). CETP is a protein responsible for lipid molecule interchange between lipoproteins, enriching VLDL in cholesterol, whereas HL regulates plasma concentration of atherogenic lipoprotein, such as intermediatedensity lipoproteins (IDL) and sLDL.

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


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