Calorie restriction reduces low grade inflammation and ameliorate outcome of Non-alcoholic fatty liver disease

2018 ◽  
Vol 56 (2) ◽  
pp. 19
Author(s):  
Ahmed Abdelsadik
2019 ◽  
Vol 10 (6) ◽  
pp. 3637-3649 ◽  
Author(s):  
Youdong Li ◽  
Jinwei Li ◽  
Qingfeng Su ◽  
Yuanfa Liu

Non-alcoholic fatty liver disease (NAFLD) is associated with low-grade chronic inflammation and intestinal dysbiosis.


Diabetologia ◽  
2019 ◽  
Vol 63 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Martijn C. G. J. Brouwers ◽  
Nynke Simons ◽  
Coen D. A. Stehouwer ◽  
Aaron Isaacs

Abstract Non-alcoholic fatty liver disease (NAFLD) is highly prevalent among individuals with type 2 diabetes. Although epidemiological studies have shown that NAFLD is associated with cardiovascular disease (CVD), it remains unknown whether NAFLD is an active contributor or an innocent bystander. Plasma lipids, low-grade inflammation, impaired fibrinolysis and hepatokines are potential mediators of the relationship between NAFLD and CVD. The Mendelian randomisation approach can help to make causal inferences. Studies that used common variants in PNPLA3, TM6SF2 and GCKR as instruments to investigate the relationship between NAFLD and coronary artery disease (CAD) have reported contrasting results. Variants in PNPLA3 and TM6SF2 were found to protect against CAD, whereas variants in GCKR were positively associated with CAD. Since all three genes have been associated with non-alcoholic steatohepatitis, the second stage of NAFLD, the question of whether low-grade inflammation is an important mediator of the relationship between NAFLD and CAD arises. In contrast, the differential effects of these genes on plasma lipids (i.e. lipid-lowering for PNPLA3 and TM6SF2, and lipid-raising for GCKR) strongly suggest that plasma lipids account for their differential effects on CAD risk. This concept has recently been confirmed in an extended set of 12 NAFLD susceptibility genes. From these studies it appears that plasma lipids are an important mediator between NAFLD and CVD risk. These findings have important clinical implications, particularly for the design of anti-NAFLD drugs that also affect lipid metabolism.


2020 ◽  
Vol 74 ◽  
pp. 377-381
Author(s):  
Agata Łukawska ◽  
Marcin Kałużny ◽  
Sonia Nogalska ◽  
Eliza Kubicka ◽  
Justyna Kuliczkowska-Płaksej ◽  
...  

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in developed countries. This condition includes benign non-alcoholic fatty liver disease and non-alcoholic steatohepatitis with possible fibrosis leading to cirrhosis and hepatocellular carcinoma. Association of NAFLD and polycystic ovary syndrome (PCOS) has been widely discussed. Women with PCOS are prone to develop NAFLD more often. PCOS is one of the most common endocrine disorders among reproductive-age women, characterized by an excess of androgens, anovulation, and polycystic ovary on ultrasound. Obesity, dyslipidemia and insulin resistance (IR) are frequently observed in women with PCOS, being also important factors predisposing to the development of NAFLD. IR may stimulate theca cells to excessive production of androgens, inhibits the production of sex hormone-binding globulin in the liver, which contributes to the increase of the bioactive form of testosterone. Hyperandrogenemia also plays an important role in NAFLD pathogenesis and progression. Androgen excess promotes visceral fat accumulation, development of dyslipidemia, IR, and contributes to low-grade inflammation. The pathophysiological associations between PCOS and NAFLD are not fully understood although it seems reasonable to screen PCOS women for the presence of NAFLD.


2019 ◽  
Vol 123 (1) ◽  
pp. 104-112
Author(s):  
Shunming Zhang ◽  
Yeqing Gu ◽  
Min Lu ◽  
Jingzhu Fu ◽  
Qing Zhang ◽  
...  

AbstractAnimal studies have suggested that mushroom intake can alleviate non-alcoholic fatty liver disease (NAFLD) due to its anti-inflammatory and antioxidant properties. However, the association between mushroom intake and NAFLD is unknown in humans. We aimed to investigate the association of mushroom intake with NAFLD among Chinese adults. This is a cross-sectional study of 24 236 adults (mean (standard deviation) age: 40·7 (sd 11·9) years; 11 394 men (47·0 %)). Mushroom intake was assessed via a validated FFQ. Newly diagnosed NAFLD was identified based on the results of annual health examinations, including ultrasound findings and a self-reported history of the disease. Multiple logistic models were used to examine the association between mushroom intake and NAFLD. The prevalence of newly diagnosed NAFLD was 19·0 %. Compared with those consuming mushrooms less frequently (≤1 time/week), the fully adjusted OR of newly diagnosed NAFLD were 0·95 (95 % CI 0·86, 1·05) for those consuming 2–3 times/week and 0·76 (95 % CI 0·63, 0·92) for those consuming ≥4 times/week (Pfor trend = 0·01). The inverse association was consistent in subgroups defined by age, sex and BMI. In conclusion, higher mushroom intake was significantly associated with lower prevalence of NAFLD among Chinese adults. Future research is required to understand the causal association between mushroom intake and NAFLD.


2021 ◽  
Vol 22 (15) ◽  
pp. 8008
Author(s):  
Mayumi Nagashimada ◽  
Masao Honda

Non-alcoholic fatty liver disease (NAFLD) is a leading cause of liver cirrhosis and hepatocellular carcinoma. NAFLD is associated with metabolic disorders such as obesity, insulin resistance, dyslipidemia, steatohepatitis, and liver fibrosis. Liver-resident (Kupffer cells) and recruited macrophages contribute to low-grade chronic inflammation in various tissues by modulating macrophage polarization, which is implicated in the pathogenesis of metabolic diseases. Abnormalities in the intestinal environment, such as the gut microbiota, metabolites, and immune system, are also involved in the pathogenesis and development of NAFLD. Hepatic macrophage activation is induced by the permeation of antigens, endotoxins, and other proinflammatory substances into the bloodstream as a result of increased intestinal permeability. Therefore, it is important to understand the role of the gut–liver axis in influencing macrophage activity, which is central to the pathogenesis of NAFLD and nonalcoholic steatohepatitis (NASH). Not only probiotics but also biogenics (heat-killed lactic acid bacteria) are effective in ameliorating the progression of NASH. Here we review the effect of hepatic macrophages/Kupffer cells, other immune cells, intestinal permeability, and immunity on NAFLD and NASH and the impact of probiotics, prebiotics, and biogenesis on those diseases.


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