Edited by:
Professor Yu-Jui Yvonne Wan, PhD, University of California-Davis, United States of America
Professor Huiping Zhou, PhD, Virginia Commonwealth University, United States of America
Professor Alfred Sze-Lok Cheng, PhD, The Chinese University of Hong Kong, China
Submission Status: Open | Submission Deadline: 31 January 2025
Cell & Bioscience is calling for submissions to our Collection on Dietary Contributions to Hepatic Diseases and Cancer. About 25% of the global population has metabolic dysfunction-associated steatotic liver disease (MASLD). Metabolic comorbidities associated with MASLD include obesity, type 2 diabetes (T2DM), and hyperlipidemia. Alarmingly, the prevalence of MASLD is 70% in T2DM patients. Further, MASLD can progress into metabolic dysfunction-associated steatohepatitis (MASH), leading to the development of hepatocellular carcinoma (HCC). Together, MASLD will be the most common cause of chronic liver disease worldwide, and there is an urgent need to have diagnostic markers or safe drugs to prevent and treat MASH.
Different diets, such as the Western, high-fat, and ketogenic, are frequently used to study dietary effects in animal models. While a high-fat diet is efficient in weight gain, a sucrose-enriched Western diet is highly inflammatory in stimulating the expansion of IL-17A-producing γδ T cells. A ketogenic diet typically consists of about 75% of calories from fat and is used to treat MAFLD in patients. However, a ketogenic diet induces MAFLD and generates insulin resistance in rodents. When a ketogenic diet is consumed, the quality of fats, potential side effects, nutritional deficiency, and long-term impacts and sustainability are concerns. Those clinical issues warrant attention.
Emerging evidence reveals that diet-induced gut dysbiosis causes metabolic diseases and systemic inflammation. Through portal circulation, the liver is heavily exposed to gut-derived metabolites. Thus, diet affects the liver's health through the gut microbiome and its associated metabolites. It is interesting to note that the incidence of MASH and HCC is gender different, and so are the profiles of the gut microbiome and bile acids. Bile acids have been recognized as the intrinsic links to explain how gut microbes affect host metabolism. The mechanism for such gender differences in MASH and HCC would be particularly interesting, as it might help us understand why women are protected from developing them. The discovery of gender-specific biomarkers for MASH and HCC would also be significant.
MAFLD-associated HCC tends to be more resistant to immune checkpoint inhibitor treatment than the viral-associated HCC. Understanding the impact of different diets and nutrients on molecular signatures and the immune landscape is essential, as it affects live carcinogenesis and HCC treatment outcomes. Furthermore, due to the significance of the gut-liver axis in affecting liver phenotype, having orthotopic HCC models developed in immune-competent animals would be essential to study liver carcinogenesis and prevention as well as treatment. The recent development of novel animal models and their usage in biomarker discovery and drug development would be important for the field. Further, any novel models, devices, and state-of-the-art technology used to advance the field of MASH and HCC would be significant and impactful.
This collection invites submissions that explore the intersections of diet, nutrition, metabolic liver diseases, and cancer. We welcome original research or review papers that provide insights into the basic, translational, and clinical aspects of metabolic liver diseases and cancer.
Image credits: HCC developed in MASH; Yu-Jui Yvonne Wan’s lab.
This collection supports and amplifies research related to SDG 2 and 3: Zero hunger and Good health and well being.