By Prof. Antonio Vidal-Puig MD, PhD, FRCP (auth.), Matej Orešič, Antonio Vidal-Puig (eds.)
The target of this booklet is to supply the objective viewers, in particular scholars of drugs, Biology, structures Biology and Bioinformatics, in addition to skilled researchers in study fields suitable to metabolic syndrome (MetS) with an outline of the demanding situations and possibilities in structures biology and the way it may be used to take on MetS. particularly, the goals are: (1) to supply an creation to the major organic techniques enthusiastic about the pathophysiology of MetS; (2) by utilizing particular examples, offer an advent to the newest applied sciences that use a structures biology method of research MetS; and (3) to offer an outline of the mathematical modeling ways for learning MetS.
The sincerely written chapters by means of major specialists within the box presents exact descriptions an important for the original place of this ebook and its concentrate on the appliance of structures biology to take on particular pathophysiologically correct features of MetS and gives a useful useful consultant to this study community.
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Additional resources for A Systems Biology Approach to Study Metabolic Syndrome
1994). In individuals with IR, ApoC-III cannot be suppressed by insulin and is promoted by increased glucose, leading to an overproduction of VLDL. Furthermore, recent studies have suggested a genotype–phenotype relationship between ApoC-III and NAFLD, showing that some single-nucleotide polymorphisms (SNPs) in the gene encoding APOC-III, may be associated with hypertriglyceridemia and MetS (Guettier et al. 2005; Miller et al. 2007; Petersen et al. 2010). In fact, the ApoC-III polymorphisms T-455C and C-482T were found associated with increased plasma ApoC-III and TG concentrations, and 3 The Liver in Metabolic Syndrome 33 with increased prevalence of NAFLD (Miller et al.
Via molecular interactions or biochemical reactions). The investigation is focusing on the elucidation of the regulation of the molecule Z, which is associated with a specific biological function. The hypothesis being investigated is that Z is controlled by the molecule X. , by knock-down), which following the experiment leads to the conclusion that indeed function of Z depends on X (Fig. 1b). However, such an approach disregards potential other networks that may regulate Z as well as modulate the function of X (Fig.
2008). In the post absorptive and fasting states the major rate of FFA delivered to the liver derived from lipolysis of peripheral tissue, mainly from adipose tissue. Lipolysis of adipose tissue is under the control of the hormone-sensitive lipase (HSL), which is an enzyme activated when the body needs to mobilize energy stores, whereas is strongly inhibited by insulin in the post prandial feeding state. Adipose tissue IR of NAFLD patients, which is characterized by the lack of suppression of lipolysis by insulin, determines increased HSL levels with a consequent deregulation of adipose-derived FFA flux to the liver in the fasting state (Mittendorfer et al.
A Systems Biology Approach to Study Metabolic Syndrome by Prof. Antonio Vidal-Puig MD, PhD, FRCP (auth.), Matej Orešič, Antonio Vidal-Puig (eds.)