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

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

The objective of this publication is to supply the objective viewers, particularly scholars of drugs, Biology, structures Biology and Bioinformatics, in addition to skilled researchers in study fields correct 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. particularly, the goals are: (1) to supply an advent to the most important organic strategies concerned with the pathophysiology of MetS; (2) by utilizing particular examples, supply an creation to the newest applied sciences that use a platforms biology method of research MetS; and (3) to offer an summary of the mathematical modeling ways for learning MetS.

The truly written chapters via top specialists within the box offers unique descriptions an important for the original place of this ebook and its concentrate on the appliance of platforms biology to take on particular pathophysiologically correct features of MetS and offers a invaluable functional advisor to this learn community.

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Extra info for A Systems Biology Approach to Study Metabolic Syndrome

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The excessive FFA release rates from adipose tissue into the systemic circulation lead to an increased availability of FAs for uptake by the liver, facilitating intrahepatic lipids accumulation, and worsening hepatic IR (Boden and Shulman 2002). Furthermore, among causes of lipid accumulation in NAFLD, a key role is also played by fatty acid transporters and their regulators, fatty acid translocase/cluster differentiation protein-36 (FAT/CD36), fatty acid transport protein (FATP) and fatty acid binding proteins (FABPs), which could further enhance hepatic lipid uptake (Greco et al.

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. PI3K activation is involved in the translocation of glucose transporter type 4 (GLUT4) to the plasma membrane, that facilitate glucose uptake and its utilization in muscle and adipose tissue. Therefore, inhibition of PI3K results in reduced glucose uptake in the organs, and in exacerbated IR.

LXRs regulate cholesterol homeostasis through the control of bile acid (BA) production (in rodents), cholesterol influx, transport and efflux, and impact energy homeostasis through the regulation of glucose metabolism (in rodents). LXRs positively regulate some aspects of BA metabolism, such as the transcription of cholesterol 7α hydroxylase (CYP7A1), which represent a rate-limiting step in BA synthesis, and the transcription of the BA-conjugating enzyme UDP-glucuronosyltransferase 1–3 (UGT1A3), which facilitate BA elimination (Barbier et al.

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