Dietary Interventions in Liver Disease
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Dietary Interventions in Liver Disease

Foods, Nutrients, and Dietary Supplements

Ronald Ross Watson, Victor R Preedy, Ronald Ross Watson, Victor R. Preedy

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eBook - ePub

Dietary Interventions in Liver Disease

Foods, Nutrients, and Dietary Supplements

Ronald Ross Watson, Victor R Preedy, Ronald Ross Watson, Victor R. Preedy

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À propos de ce livre

Dietary Interventions in Liver Disease: Foods, Nutrients, and Dietary Supplements provides valuable insights into the agents that affect metabolism and other health-related conditions in the liver. It provides nutritional treatment options for those suffering from liver disease. Information is presented on a variety of foods, including herbs, fruits, soy and olive oil, thus illustrating that variations in intake can change antioxidant and disease preventing non-nutrients that affect liver health and/or disease promotion. This book is a valuable resource for biomedical researchers who focus on identifying the causes of liver diseases and food scientists targeting health-related product development.

  • Provides information on agents that affect metabolism and other health-related conditions in the liver
  • Explores the impact of composition, including differences based on country of origin and processing techniques
  • Addresses the most positive results from dietary interventions using bioactive foods to impact liver disease, including reduction of inflammation and improved function

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Informations

Éditeur
Academic Press
Année
2019
ISBN
9780128144671
Section IV
Dietary Macronutrients and Micronutrients for Healthy Liver Function
Chapter 17

Major Dietary Interventions for the Management of Liver Disease

Idris Adewale Ahmed Department of Biotechnology, Faculty of Science, Lincoln University College Malaysia, Petaling Jaya, Malaysia

Abstract

The liver is a major organ of the body with multiple functions such as regulation, metabolism, synthesis, and storage. Hepatic injury, however, causes irreversible impairment of liver function and changes in its architecture and blood supply. The major causes of hepatic injury and chronic liver diseases are nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), chronic hepatitis B virus and hepatitis C virus infections, and hepatocellular carcinoma. Liver diseases have thus become a global health burden, and the spectrum of disease of both ALD and NAFLD includes steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and end-stage liver disease. There are no approved pharmacological treatments for NAFLD worldwide, the use of various dietary interventions, however, has the potential to mitigate the risks of both NAFLD- and NASH-related complications. Such dietary interventions include, but not limited to, the Mediterranean diet; Japanese traditional diet; probiotics; vitamins C, D, and E; quercetin; epigallocatechin-3-gallate; and resveratrol.

Keywords

Alcoholic liver disease; Hepatitis infections; Hepatocellular carcinoma (HCC); Nonalcoholic fatty liver disease; Steatohepatitis; Steatosis

1. Introduction

The liver plays a crucial role in the regulation of protein, fat, and carbohydrate metabolism as well as vitamin storage and activation, detoxification, and excretion of waste products, to mention but a few. The disruption of these processes due to chronic liver disease (CLD), however, results in improper nutrient digestion, absorption, usage, and ultimately malnutrition.1 Furthermore, the liver also has a substantial antioxidant defense, such as the tripeptide glutathione, to prevent the damaging effects of free radicals which are generated as an ultimate consequence of the aerobic existence during normal physiology. However, in pathophysiological conditions, the balance between the generation of free radicals and the liver capacity to detoxify them is shifted to give rise to oxidative stress that negatively influences cellular homeostasis and organelle function.2 In other words, hepatic injury causes irreversible impairment of liver function and changes in its architecture and blood supply.
Liver diseases have undoubtedly become a global health burden. One of the most common and deleterious conditions of liver diseases is CLD, which is a progressive destruction of the hepatic parenchyma for a period greater than 6 months which eventually leads to liver fibrosis, cirrhosis, and potentially hepatocellular carcinoma (HCC).3 The chronic liver disease is marked by an impaired synthesis of serum proteins and clotting factors, impaired bile secretion and cholestasis, and compromised glycemic control and ammonia metabolism.1 Liver cirrhosis, in particular, is the ninth leading cause of death in Western countries. While chronic viral hepatitis (CVH) and excessive alcohol consumption remain the most common causes of CLD, other causes of CLD are nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, and HCC.3
Specifically, alcohol is the most widely used drug which is responsible for the liver injury. The three most common histological forms of alcoholic liver injury are fatty liver (steatosis), alcoholic hepatitis, and finally fibrosis or cirrhosis. Similarly, the spectrum of disease of NAFLD includes steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and end-stage liver disease.4 In other words, both ALD and non-ALD s mostly share a common but wide spectrum of diseases.5 Inflammation, however, is a crucial part of both acute and chronic liver disorders including fatty liver diseases such as ALD and NAFLD.6
According to the literature, multiple hits, rather than the previously thought two-hit hypothesis, are involved in the progression of liver damage in both NAFLD and ALD. The key events during the progression are inflammation, dysregulated angiogenesis, and fibrosis, which are closely interconnected. In addition, activated hepatic stellate cells (HSCs) are responsible for the sustenance of the extracellular matrix (ECM) remodeling and collagen deposition, which in turn, is followed by advanced fibrosis, which is associated with increased risk of HCC development.5
While fibrogenesis occurs in the liver as a protective response to chronic liver injury, the causes include chronic hepatitis B or hepatitis C infection, congenital abnormalities, chemical intoxication, drug toxicity, excess alcohol consumption, NAFLD, parasitic diseases, and biliary atresia. Furthermore, liver fibrosis which is the progressive deposition of ECM proteins in the liver, in combination with vascular remodeling, is responsible for cirrhosis and HCC. There is interplay among hepatocytes, macrophages, and HSCs during the development...

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