Studies have found that intermittent fasting (IF) can prevent diabetes, cancer, heart disease, and neuropathy, while in humans it has helped to alleviate metabolic syndrome, asthma, rheumatoid arthritis, Alzheimer's disease, and many other disorders. IF involves a series of coordinated metabolic and hormonal changes to maintain the organism's metabolic balance and cellular homeostasis. More importantly, IF can activate hepatic autophagy, which is important for maintaining cellular homeostasis and energy balance, quality control, cell and tissue remodeling, and defense against extracellular damage and pathogens. IF affects hepatic autophagy through multiple interacting pathways and molecular mechanisms, including adenosine monophosphate (AMP)-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), silent mating-type information regulatory 2 homolog-1 (SIRT1), peroxisomal proliferator-activated receptor alpha (PPARα) and farnesoid X receptor (FXR), as well as signaling pathways and molecular mechanisms such as glucagon and fibroblast growth factor 21 (FGF21). These pathways can stimulate the pro-inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α), play a cytoprotective role, downregulate the expression of aging-related molecules, and prevent the development of steatosis-associated liver tumors. By influencing the metabolism of energy and oxygen radicals as well as cellular stress response systems, IF protects hepatocytes from genetic and environmental factors. By activating hepatic autophagy, IF has a potential role in treating a variety of liver diseases, including non-alcoholic fatty liver disease, drug-induced liver injury, viral hepatitis, hepatic fibrosis, and hepatocellular carcinoma. A better understanding of the effects of IF on liver autophagy may lead to new approaches for the prevention and treatment of liver disease.

Primary liver carcinoma is the sixth most common cancer worldwide, while hepatocellular carcinoma (HCC) is the most dominant cancer type. Chronic hepatitis B and C virus infections and aflatoxin exposure are the main risk factors, while nonalcoholic fatty liver disease caused by obesity, diabetes, and metabolic syndrome are the more common risk factors for HCC. Metabolic disorders caused by these high-risk factors are closely related to the tumor microenvironment of HCC, revealing a possible cause-and-effect relationship between the two. These metabolic disorders involve many complex metabolic pathways, such as carbohydrate, lipid, lipid derivative, amino acid, and amino acid derivative metabolic processes. The resulting metabolites with significant abnormal changes in the concentration level in circulating blood may be used as biomarkers to guide the diagnosis, treatment, or prognosis of HCC. At present, there are high-throughput technologies that can quickly detect small molecular metabolites in many samples. Compared to tissue biopsy, blood samples are easier to obtain, and patients’ willingness to participate is higher, which makes it possible to study blood HCC biomarkers. Over the past few years, a substantial body of research has been performed worldwide, and other potential biomarkers have been identified. Unfortunately, due to the limitations of each study, only a few markers have been widely verified and are suitable for clinical use. This review briefly summarizes the potential blood metabolic markers related to the diagnosis of HCC, mainly focusing on amino acids and their derivative metabolism, lipids and their derivative metabolism, and other possible related metabolisms.

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor worldwide, characterized by high malignancy and rapid progression. Most cases are diagnosed at intermediate to advanced stages. Current treatment methods have limited efficacy, resulting in high recurrence rates and poor prognosis. Radical hepatectomy remains the primary treatment for HCC, complemented by radiotherapy, chemotherapy, targeted therapy, and immunotherapy. Despite significant improvement in patient prognosis with radical hepatectomy, the five-year survival rate post-surgery remains low; thus necessitating exploration of more effective therapeutic approaches. Ferroptosis is a recently discovered form of cell death that can modulate the occurrence and development of HCC through various mechanisms. This article aims to elucidate the mechanism of ferroptosis and its impact on HCC development to provide novel insights for diagnosis and treatment.

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), previously known as Nonalcoholic Fatty Liver Disease (NAFLD), is characterized by an abnormal accumulation of fat in the liver. The causes of MASLD are varied, and include an unhealthy lifestyle, hyperlipidemia, hypertension, and type 2 diabetes mellitus. They are considered to be susceptibility-inducing factors for MASLD, and are strongly associated with obesity. Many researchers have explored the pathogenesis of MASLD in recent years, and have concluded that its development is associated with insulin resistance and impaired fat metabolism, which manifests as a form of metabolic liver injury. Currently available treatments remain challenging to implement, and impose a significant burden on the healthcare system. Neutrophils play an important role in the development of MASLD, and are crucial immune cells that provide the first line of defense against infection and injury. This review examines the pathogenesis of MASLD and the role of neutrophils in the disease, and further explores current advances in MASLD treatment as well as the therapeutic potential of neutrophils.