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Liver, Biliary Tract and Pancreatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Risk factors for fatty liver are: Alcoholic fatty liver disease: AlcoholNon-alcoholic fatty liver disease: ObesityType 2 diabetesMetabolic syndromeDyslipidemiaLess common: DILI, hypothyroidism, obstructive sleep apnoea, hypopituitarism, hypogonadism, polycystic ovary syndrome, pancreatoduodenal resection and psoriasis
Weight and health
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Non-alcoholic fatty liver disease occurs because of an accumulation of fat in the liver. Not only does this damage the liver, but it is linked to developing type 2 diabetes, high blood pressure and kidney disease.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The development of alcoholic fatty liver is influenced by dietary factors354,357 In normal volunteers given measured amounts of alcohol, more fatty change developed with normal fat diets than with low-fat diets. Replacement of triglycerides containing long-chain fatty acids with triglycerides containing medium-chain fatty acids showed that the ability of alcohol to produce liver fat accumulation is markedly reduced.
Low-intensity exercise diverts cardiac fatty acid metabolism from triacylglycerol synthesis to beta oxidation in fructose-fed rats
Published in Archives of Physiology and Biochemistry, 2023
Milan Kostić, Goran Korićanac, Snežana Tepavčević, Jelena Stanišić, Snježana Romić, Tijana Ćulafić, Tamara Ivković, Mojca Stojiljković
High consumption of fructose may cause problems due to its lipogenic potential (Herman and Samuel 2016). A significant increase in hepatic de novo lipogenesis is one of the major adverse causes for metabolic burden under high fructose consumption. It leads to hepatic lipid accumulation and non-alcoholic fatty liver disease. In addition, increased plasma triacylglycerols (TAG) and very-low-density lipoprotein (VLDL) – TAG levels induce TAG accumulation in extrahepatic tissues, leading to lipotoxicity and insulin resistance in response to high fructose consumption. Fructose-induced lipotoxicity leads to autophagy in skeletal muscle, cardiac dysfunction, adipose tissue inflammation, chronic kidney diseases, pancreatic islet dysfunction, brain oxidative stress and inflammation (reviewed in Zhang et al.2017). This diet is also accompanied by the development of insulin resistance in the heart (Zakula et al.2011, Stanišić et al.2016) and it could change the use of cardiac energy substrates towards increased fatty acid (FA) uptake and catabolism (Coort et al.2007, Zhang et al.2017).
Jiang Zhi Granule protects immunological barrier of intestinal mucosa in rats with non-alcoholic steatohepatitis
Published in Pharmaceutical Biology, 2021
Xiao Yu, Haiyan Zhang, Jielu Pan, Lu Zou, Ling Tang, Hongyu Miao, Peiyong Zheng, Lianjun Xing
A clinical syndrome with the umbrella term non-alcoholic fatty liver disease (NAFLD) has been characterized via hepatic steatosis of parenchyma and storage of fat without any history of excessive drinking of alcohol (Patel et al. 2011). It encompasses a spectrum of diseases with its pathogenesis mainly associated with insulin resistance (IR) and metabolic syndrome (MS) (Alkhouri et al. 2010). The incidence of liver steatosis has been reported to increase annually probably because of changes in living standards of individual. Clinically, NAFLD progresses from simple steatosis to non-alcoholic steatohepatitis (NASH), which culminates in liver cirrhosis and even hepatocellular carcinoma (Lombardi et al. 2017). The main risk factors for the development of NASH are obesity, hypertension, hypertriglyceridaemia and IR (Lo et al. 2015; Younossi et al. 2018). Usually, patients with NASH often develop fibrosis and cirrhosis with its pathogenesis being extremely complex. The theory of ‘two strikes’ put forward by Day (Wang et al. 2015) has become the main hypothesis to elucidate the pathogenesis of the disease. Based on various reasons, the first hypothesis suggested that increased accumulation of lipids in liver culminated in the occurrence of simple steatosis. The second theory indicates that an increase in the generation of free radicals and lipid peroxidation could result in the overproduction of some cytokines, which may directly damage hepatocytes and cause inflammation and necrosis.
Downregulation of mitogen-activated protein kinases (MAPKs) in chronic ethanol-induced fatty liver
Published in Toxicology Mechanisms and Methods, 2020
Fang-Fang Guo, Mo Xiao, Shao-Yi Wang, Tao Zeng, Lei Cheng, Qing Xie
Alcohol abuse remains to be one of the major causes of chronic liver diseases in developed and underdeveloped countries. The most common and earliest manifestation of ethanol-induced liver damage is the accumulation of fat in hepatocytes, namely alcoholic fatty liver (AFL), which can be induced by binge drinking and also chronic ethanol consumption. Although AFL is usually reversible and without apparently noticeable symptoms, accumulating evidences have indicated that the fatty liver are vulnerable to various toxicants such as the acetaminophen and inorganic arsenic (Wu et al. 2008; Kucera et al. 2012). More importantly, there is evidence suggesting that AFL could progress into advanced alcoholic fibrosis and cirrhosis after abstinence (Leevy 1962; Sørensen et al. 1984). As AFL develops in over 90% of individuals who drink more than 60 g/day of alcohol, and effective treatment is still lacking (Ki et al. 2007; O'Shea et al. 2010), much more works are urgently needed to clarify the underlying mechanisms of AFL.