Ami Schattner's Metabolic Aspects of Chronic Liver Disease PDF

By Ami Schattner

ISBN-10: 1600212018

ISBN-13: 9781600212017

ISBN-10: 1606927523

ISBN-13: 9781606927526

This publication discusses intimately new points of the metabolic foundation of significant persistent liver ailments. Entities corresponding to non-alcoholic fatty liver ailment (fatty liver and Non-Alcoholic SteatoHepatitis - NASH), diabetes in power hepatitis C, hemochromatosis, Wilson's affliction, Gaucher ailment, porphyria, in addition to liver cirrhosis and its metabolic results could be mentioned intimately. those scientific stipulations are hugely primary and impact hundreds of thousands of sufferers within the united states and world-wide. for instance, non-alcoholic fatty liver sickness is the most typical explanation for increased liver enzymes within the normal inhabitants. This box has been essentially reworked during the last few years, with many new insights won, relating to either pathogenesis and potent novel remedies.

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Extra info for Metabolic Aspects of Chronic Liver Disease

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These studies also showed that obese mice with fatty liver clear endotoxin less than nonobese controls [163]. This additional stressor is sometimes referred to as a “second hit” in a paradigm that identifies the accumulation of fat as the “first hit” [165]. Possible candidates for the second hit include increased oxidative stress, lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal, decreased antioxidants, Pathophysiology of NASH 19 adipocytokines, transforming growth factor-β (TGF-β), Fas ligand, mitochondrial dysfunction, fatty acid oxidation by CYPs (CYP 2E1, 4A10, and 4A14), and peroxisomes, excess iron, small intestinal bacterial overgrowth, and the generation of gut-derived toxins such as lipopolysaccharide and ethanol [1,97,165].

Figure 3. Sources and fates of liver fat. The major sources of fat in the liver are delivery as NEFA from adipose tissue and de novo lipogenesis from carbohydrates and amino acids. Short chain NEFA from the gut are a small fraction of total circulating NEFA in the fed state. Uptake of triglyceride in the form of LDL and IDL constitutes a minor fraction. The intrahepatic NEFA pool has two major fates. Some undergoes mitochondrial β-oxidation while most is generally re-esterified to triglyceride, incorporated into VLDL and secreted into the circulation.

A recently described rat model of feeding high-fat liquid diet (71% of energy from fat which included corn, olive, and safflower oil) for 3 weeks was reported as resemble human NASH [144]. These Sprague-Dawley rats exhibited many of the features of human NASH that included obesity, insulin resistance, hyperinsulinemia, increased hepatic TNF-α mRNA expression, induced CYP2E1 and increased CYP2E1 mRNA expression, morphologically abnormal mitochondria, increased both oxidative stress and lipid peroxidation, fatty liver, patchy inflammation, and increased collagen in the liver.

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Metabolic Aspects of Chronic Liver Disease by Ami Schattner

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