Non Alcohol Fatty Liver Disease – The accuracy of FIB-4 for the detection of liver stiffness measurements in patients with non-alcoholic fatty liver disease: A cross-sectional study in reference centers.

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Non Alcohol Fatty Liver Disease

Non Alcohol Fatty Liver Disease

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Do All Heavy Drinkers Develop Alcoholic Fatty Liver Disease (afld)?

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By Xiangyu Guo Xiangyu Guo Scilit Google Scholar View Publications 1, 2, Xunzhe Yin Xunzhe Yin Scilit Google Scholar View Publications 1, Zuojia Liu Zuojia Liu Scilit Google Scholar View Publications 1, * and Jin Wang Jin Wang Scilit Google Scholar View Publications 3, *

Figure 1 From Knowing What’s Out There: Awareness Of Non Alcoholic Fatty Liver Disease

State Key Laboratory of Electroanalytical Chemistry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China

Received: 2 November 2022 / Revised: 29 November 2022 / Accepted: 2 December 2022 / Published: 7 December 2022

(For the Special Issue Nonalcoholic Fatty Liver Disease/Metabolic Associated Fatty Liver Disease: New Insights 2.0)

Non Alcohol Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic lung disease, affecting a quarter of the world’s population, and has become a major public health problem. NAFLD is a clinicopathological disease characterized by hepatic steatosis, independent of ethanol and other harmful substances. Recent studies have shown that the development of NAFLD is associated with lipid accumulation, oxidative stress, endoplasmic reticulum stress, and lipotoxicity. Various natural products have been shown as regulators of NAFLD in vivo and in vitro. This paper describes the pathogenesis of NAFLD and some natural products that have shown therapeutic effects in NAFLD. Our work suggests that natural products may be a viable therapeutic option for NAFLD.

Pdf] Current Guidelines For The Management Of Non Alcoholic Fatty Liver Disease: A Systematic Review With Comparative Analysis

Non-alcoholic fatty liver disease (NAFLD) has evolved from an unknown disease into the most common cause of liver disease worldwide. Currently, the consensus defines NAFLD as an umbrella term for diseases in which steatosis occurs in more than 5% of hepatocytes with metabolic risk factors (especially obesity and diabetes type 2), without alcoholism or other liver diseases. 1, 2]. NAFLD is divided into non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH) according to histological features (Figure 1) [3]. NAFL was defined as all cases characterized by steatosis, with no or mild lobular inflammation. In contrast, NASH is characterized by the presence of hepatocellular damage (hepatocyte ballooning degeneration, diffuse lobular inflammation and fibrosis). Although simple steatosis is considered a “benign” disease, its combination with liver fibrosis can lead to the development of cirrhosis and hepatocellular carcinoma (HCC) [ 4 , 5 ]. Therefore, NAFLD is considered an important factor in regulating mortality from liver-related diseases.

With the global increase in metabolic syndrome, obesity and diabetes, the prevalence of NAFLD has increased dramatically, affecting a quarter of the world’s population [ 6 ]. A global epidemiological meta-analysis in 2016 showed the prevalence of NAFLD in all countries [7]. This may be due to differences in total caloric intake, physical activity, body fat distribution, socioeconomic status and body composition, which are highest in the Middle East and lowest in Africa, with about 31.79% (95% confidence interval (CI), 13.48- 58.23) and 13.48% (95% CI, 5.69–28.69), respectively [7]. In this study, metabolic diseases associated with NAFLD, including obesity 51.34% (95% CI, 41.38-61.20), type 2 diabetes 22.51% (95% CI, 17.92-27.89), hyperlipidemia 69.16% (95 % CI, 49.96%). ), hypertension 39.34% (95% CI, 33.15-45.88) and metabolic syndrome 42.54% (95% CI, 30.06-56.05), all showed strong relationships [ 7 ]. Obesity and insulin resistance (IR) lead to impaired lipid metabolism and chronic inflammation, which can lead to the progression of NAFLD to NASH and even cirrhosis, HCC and death. Statistical analysis showed a global prevalence of 59.1% (95% CI, 47.6-69.7) of NASH among patients with NAFLD biopsied [7]. Patients with NAFLD are the fastest growing group of HCC patients requiring liver transplantation in the United States. A study on the etiology of HCC was recorded from 2002-2012 and found an increase in HCC related to NASH from 8.3% in 2002 to 13.5% in 2012 [8]. As a result, NAFLD has become an untreatable global health problem.

In clinical practice, patients with NAFLD show high triglycerides, high LDL and reduced HDL in biochemical tests [9]. Symptoms are often associated with features of the metabolic syndrome, such as obesity, dyslipidemia, type 2 diabetes and hypertension [2, 7, 10, 11, 12]. However, the pathogenesis of NAFLD is not known, and this has become an obstacle in the treatment of NAFLD. Previous studies show that IR and hepatic steatosis due to excess fat are the “first-hit”, but the hepatocytes suffer damage, inflammation, fibrosis and other pathological changes. due to oxidative stress and lipid peroxidation to create a “double-hit” [ 13 ]. Today, the “multiple-hit” theory is widely accepted, based on the “second-hit” theory, which includes various factors such as oxidative stress, endoplasmic reticulum (ER) stress and lipotoxicity [14]. This theory provides the most accurate explanation for the pathogenesis of NAFLD.

Currently, there is no approved treatment for NAFLD, and treatment is through diet and lifestyle changes [15]. However, patients with NAFLD often have difficulty maintaining a healthy lifestyle. Therefore, it is important to strengthen research on the pathogenesis of NAFLD and find safe and effective drugs for the prevention and treatment of NAFLD. With “NAFLD” and “Natural products” as key words, we searched the PubMed database for relevant literature from the past ten years. It is known that the effects of natural products have been repeatedly evaluated in different signaling pathways related to lipid metabolism, oxidative stress, ER stress and lipotoxicity, and show excellent therapeutic results. In this article, we review activities related to the pathogenesis of NAFLD and some natural small molecule compounds that have been shown to play a therapeutic role in NAFLD, as well as some natural compounds that may hold promise for NAFLD.

Non Alcoholic Fatty Liver Disease: A Clinical Update

When there is more energy than is consumed, the excess energy is stored in the form of lipids. In a bad situation, lipids are stored in other parts of the body [12, 16, 17, 18]. NAFLD is a classic example of ectopic accumulation of lipids (Figure 2). Hepatic steatosis in NAFLD is caused by excessive triglyceride (TG) synthesis in hepatocytes, with 60% of the substrate for this synthesis coming from white adipose tissue (WAT), 26% from de novo lipogenesis (DNL) and with 15% from eating a diet high in fat and/or high sugar [19, 20, 21].

Insulin has an anti-lipolytic effect, affects the storage of TG in adipose tissue, and promotes the esterification and storage of fatty acids [22]. Therefore, insulin resistance (IR) becomes an important therapeutic factor in NAFLD. Adipose tissue is stored in the lipid droplets of WAT as TG [23]. Lipid droplets have long been used as an inert lipid reservoir [24]. They act like a battery to store excess energy and release it when needed. In the IR state, the antilipolytic effect of insulin is reduced and the WAT is broken down, leading to an increased release of fatty acids (FFAs) [25]. Then, excess FFAs are stored in the liver as TG, causing ectopic lipid deposits and NAFLD [26].

DNL is a major pathway that promotes lipid accumulation and is associated with IR [27]. DNL is modulated by sterol regulatory element-binding protein 1c (SREBP-1c) and carbohydrate response element-binding protein (ChREBP) [ 28 , 29 ]. IR activates SREBP-1c to promote DNL in hepatocytes [ 30 , 31 ]. Glucose increases ChREBP to regulate the expression of acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), thereby promoting DNL in hepatocytes [32, 33, 34].

Non Alcohol Fatty Liver Disease

Along with the obesity epidemic, we have found that dietary factors play an important role in the development of NAFLD [35, 36, 37]. A study showed that a high-fat diet (HFD) alone led to obesity, IR and some degree of fatty tissue with less fat and fibrosis, but a diet with added fructose to increased gene expression for liver fibrosis, inflammation, ER stress and adipocyte. apoptosis. [38]. Also, animal models and

Quality Standards For The Management Of Non Alcoholic Fatty Liver Disease ( Nafld): Consensus Recommendations From The British Association For The Study Of The Liver And British Society Of Gastroenterology Nafld Special Interest Group

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