Non-alcoholic fatty liver disease – A global public health perspective

Background & Aims Nonalcoholic fatty liver disease encompasses isolated steatosis or nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH). NASH develops from isolated steatosis with obscure driving forces. We aim to identify key factors promoting this transition. Methods Following 21‐week of high‐fat diet feeding, obese mice were classified into two groups termed as isolated steatosis and NASH based on hematoxylin‐eosin staining of liver histology. The integrated multi‐omics analysis of lipidome, transcriptome and gut microbiome were performed in mice with isolated steatosis and NASH, and confirmed in human samples. Results Livers in mice with NASH lost most lipids, and the transcriptional landscape was also changed dramatically in mice with NASH in relative to mice with isolated steatosis. Plasma lipidome analysis demonstrated a very clear difference between these two groups of mice, which was partially recapitulated in serum of patients with isolated steatosis and NASH. The microbiota composition revealed that Bacteroides genus and Bacteroides uniformis species decreased while Mucispirillum genus and Mucispirillum schaedleri species increased largely in mice with NASH. More importantly, we found that Bacteroides uniformis correlated positively with triglycerides (TGs) and negatively with free fatty acids (FFAs) and PE(18:1/20:4), while Mucispirillum schaedleri correlated positively with FFAs, LysoPC(20:3), LysoPC(20:4) and DG(16:1/18:2). Mechanically, administration of Bacteroides uniformis increased specific TGs, and decreased hepatic injury and inflammation in diet‐induced mice. Conclusions Overall, through multi‐omics integration, we identified a microbiota‐lipid axis promoting the initiation of NASH from isolated steatosis, which might provide a novel perspective on NASH pathogenesis and treatment.

Section: Discussionmentioning

confidence: 99%

Coordinated changes of gut microbiome and lipidome differentiates nonalcoholic steatohepatitis (NASH) from isolated steatosis

Qian

Yao

et al. 2019

“…This diet is generally hypercaloric with inadequate intake of fruits, vegetables, whole grains, legumes, fish and low‐fat dairy products and excessive refined and processed foods, alcohol, salt, red meats, sugary beverages, snacks, eggs and butter. In addition to the role of the different foods found in the diet, the excess amount of calories are a risk factor for NAFLD …”

Section: From Major Foods Groups To Dietary Patterns: Evidence From Nmentioning

confidence: 99%

“…Non‐alcoholic fatty liver disease (NAFLD) is a major health problem because of its high prevalence. Non‐alcoholic fatty liver disease is associated with obesity, insulin resistance, type 2 diabetes mellitus (DM2), hyperlipidemia, hypertension and metabolic syndrome . Non‐alcoholic fatty liver disease covers a wide pathological spectrum ranging from steatosis to steatohepatitis (NASH) progressing to different degrees of liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC).…”

Section: Introductionmentioning

confidence: 99%

The role of nutrition in non‐alcoholic fatty liver disease: Pathophysiology and management

Berná

Romero–Gómez

2020

144

130

A healthy diet together with physical activity could induce weight loss and control the progression of non‐alcoholic fatty liver disease (NAFLD). However, the composition of diet has not been clearly established. Macronutrients such as saturated fatty acids (SFA), trans‐fats, simple sugars and animal proteins have a harmful effect on the liver. On the other hand, monounsaturated fats (MUFAs), polyunsaturated (PUFAs) omega‐3‐fats, plant‐based proteins and dietary fibres are considered to be beneficial to the liver. The impact of specific micronutrients is less well‐known. Nutrients are part of the food we eat. Food makes up our meals, which compose our dietary patterns. Non‐alcoholic fatty liver disease patients usually follow Western diets which are rich in soda, frozen junk food, juice, red meat, lard, processed meats, whole fat dairy foods, fatty snack foods, take‐away foods, cakes and biscuits and poor in cereals, whole grains, fruit, vegetables, extra virgin olive oil (EVOO) and fish. On the other hand, the Mediterranean diet (MD) is beneficial for NAFLD even when it is iso‐caloric or there are no changes in body weight. A new approach, called ‘nutritional geometry’ considers the importance of integrating nutrition, animals and the environment. The goal of this approach is to combine nutrients and foods in a model to understand how food components interact to regulate the properties of diets affecting health and disease. The use of algorithms developed by artificial intelligence (AI) to create a personalized diet for patients can provide customized nutritional counselling to prevent and treat NAFLD.

“…NAFLD is now recognized as the most common liver disease worldwide with a global prevalence of 25%‐33% . It is therefore highly likely that chronic HBV infection and NAFLD will co‐exist in many patients.…”

Section: Discussionmentioning

confidence: 99%

“…This includes co‐infection with chronic hepatitis C virus (HCV) or hepatitis D virus, chronic alcohol use and non‐alcoholic fatty liver disease (NAFLD). NAFLD is now recognized as the most common cause of liver disease worldwide and is estimated to be present in up to 25%‐33% of the global population . Virtually no countries are exempt from NAFLD with the highest prevalence now reported from countries in the Middle East.…”

Section: Introductionmentioning

confidence: 99%

Approach to the patient with chronic hepatitis B and decompensated cirrhosis

Shiffman

2020

Patients with chronic hepatitis B virus (HBV) can develop progressive fibrosis, cirrhosis and hepatocellular carcinoma. Patients with chronic HBV and cirrhosis are at risk of developing hepatic decompensation and have high mortality without antiviral therapy and/or liver transplantation. Treatment of chronic HBV with antiviral therapy is indicated in all patients with cirrhosis whatever the HBe‐antigen status and serum alanine aminotransferase (ALT), so that hepatic decompensation can be prevented. Initiating antiviral therapy in patients with decompensated cirrhosis can improve liver function, Child‐Turcotte‐Pugh (CTP) and model for end‐stage liver disease (MELD) scores, as well as the need for liver transplantation and mortality. Patients with chronic HBV and cirrhosis who do not respond to antiviral therapy with normalization of ALT may have a co‐existent liver disorder. One of the most common co‐existent liver disorders present in patients with chronic HBV is non‐alcoholic fatty liver disease (NAFLD). Patients with chronic HBV, NAFLD and cirrhosis may be at risk of developing decompensated cirrhosis and require a liver transplant. If patients with chronic HBV require liver transplantation, infection of the liver graft with HBV can be prevented with antiviral therapy.