Fanlian Huazhuo Formula alleviates high-fat diet-induced non-alcoholic fatty liver disease by modulating autophagy and lipid synthesis signaling pathway

Considering the bidirectional crosstalk along the gut-liver axis, gut-derived microorganisms and metabolites can be released into the liver, potentially leading to liver injury. In this editorial, we comment on several studies published in the recent issue of the World Journal of Gastroenterology . We focus specifically on the roles of gut microbiota in selected gastrointestinal (GI) diseases that are prevalent, such as inflammatory bowel disease, metabolic dysfunction-associated steatotic liver disease, and hepatitis B virus-related portal hypertension. Over the past few decades, findings from both preclinical and clinical studies have indicated an association between compositional and metabolic changes in the gut microbiota and the pathogenesis of the aforementioned GI disorders. However, studies elucidating the mechanisms underlying the host-microbiota interactions remain limited. The purpose of this editorial is to summarize current findings and provide insights regarding the context-specific roles of gut microbiota. Ultimately, the discovery of microbiome-based biomarkers may facilitate disease diagnosis and the development of personalized medicine.

Gut microbiota in gastrointestinal diseases: Insights and therapeutic strategies

Jiang,

Fan

2024

Potential of traditional Chinese medicine in the treatment of nonalcoholic fatty liver disease: A promising future

Zhang,

Wang,

Xie

2024

In this editorial, we provide insights into the publication by Niu et al featured in the latest edition of the World Journal of Gastroenterology . Specifically, our focus was on exploring the potential of traditional Chinese medicine (TCM) in treating nonalcoholic fatty liver disease (NAFLD) induced by a high-fat diet through various mechanisms. NAFLD is a common liver condition, affecting approximately 25% of the world's population. It is closely linked to metabolic syndrome, insulin resistance, excessive body weight, and irregular lipid processing, leading to fat accumulation in the liver, as well as oxidative stress and inflammation. While maintaining a healthy diet and active lifestyle are essential for managing NAFLD, treatment options are limited due to undefined pathogenesis and a lack of specific medications. TCM, rooted in traditional Chinese practices, presents a promising alternative through its "syndrome differentiation and treatment" principles, enhancing liver lipid metabolism, reducing inflammation, and addressing fibrosis. Certain herbs, such as Poria cocos , Puaria lobata , and Salvia miltiorrhiza , have shown significant efficacy in reducing fat deposition and improving liver function. Due to systematic research and analysis of mechanisms, TCM is anticipated to yield new approaches to prevent and treat NAFLD, increasing its clinical application.

Fanlian Huazhuo Formula: A promising herbal preparation for metabolic liver disease

Singla

2024

The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has increased significantly in recent decades and is projected to increase further due to the rising obesity rates. MASLD patients are at higher risk of developing advanced liver diseases “cirrhosis and hepatocellular carcinoma” as well as liver- or cardiovascular-related mortality. Existing lipid-lowering therapies failed to reduce the risk of mortality in these patients. Therefore, there is an urgent need for pharmacotherapies that can control and even reverse this disease. Fanlian Huazhuo Formula (FLHZF) is a combination herbal preparation, and its various individual constituents regulate hepatic lipid metabolism, adipose tissue inflammation, and gut microbiota. Despite, these useful effects, limited information is available on its benefits in diet-induced hepatosteatosis. In this article, we discuss the research findings recently published about the therapeutic effects of FLHZF in suppressing MASLD development and underlying mechanisms. Utilizing a series of in vitro and in vivo experiments, the authors demonstrated for the first time that FLHZF suppresses MASLD in male mice possibly by inhibiting hepatic de novo lipogenesis pathways and reducing hepatocyte death. This study paves the way for future investigations aimed at investigating FLHZF’s role in inhibiting lipogenesis particularly using radioactively-labeled glucose and acetate, and governing hepatocyte mitochondrial function, gut microbiome profile, and its effects in other models of MASLD, and female mice.