The treatment goals for fatty liver disease are to reduce liver fat accumulation, prevent the progression of the disease to liver fibrosis or cirrhosis, and lower the risk of cardiovascular diseases. Currently, there are no specific medications approved for use, so the treatment focus is on controlling metabolic abnormalities and improving liver metabolism. Physicians will develop personalized treatment plans based on whether the patient has conditions such as diabetes, obesity, or dyslipidemia.
Treatment strategies must combine medical monitoring with lifestyle adjustments, and regular follow-up on liver function and fat content changes is necessary. Severe cases may require evaluation for invasive treatments, but the vast majority of patients still rely on non-pharmacological interventions as the primary treatment route. The involvement of a multidisciplinary medical team (including nutritionists and exercise therapists) can significantly enhance treatment effectiveness.
Current treatments are divided into pharmacological therapies that directly target liver fat and non-pharmacological strategies that indirectly improve systemic metabolic abnormalities. Pharmacological treatments mainly target factors related to metabolic syndrome rather than directly dissolving liver fat. Non-pharmacological treatments are the core foundation, particularly effective in the early stages to prevent disease progression.
Treatment options must consider the type of fatty liver: alcoholic fatty liver requires prioritizing alcohol cessation, while non-alcoholic fatty liver disease (NAFLD) must address insulin resistance and metabolic issues. Patients with severe fibrosis may need to evaluate liver tissue biopsy to assess treatment effectiveness, and drug choices must exclude contraindications related to liver metabolic abnormalities.
Currently, the number of medications approved by the Food and Drug Administration is still limited, but the following drugs are considered potential options in clinical practice:
Experimental drugs include ACAT1 inhibitors and FXR receptor agonists, which can directly regulate liver lipid metabolism pathways. Clinical trials have shown that the FXR agonist obeticholic acid can reduce liver fibrosis indices, but monitoring for side effects related to bile salt metabolism abnormalities is necessary.
Invasive treatments are currently only used for extreme cases:
Alternative therapies require rigorous evaluation; the efficacy of herbal supplements such as milk thistle has not been confirmed and may interact with medications. All invasive treatments must assess the patient's overall metabolic status and surgical risks.
A low-carbohydrate diet (<50% of caloric intake) can effectively reduce liver fat, and the Mediterranean diet, rich in Omega-3 fatty acids and fiber, has been shown to improve non-alcoholic fatty liver indices. Trans fats and refined sugars should be avoided, and it is recommended that 15-20% of daily caloric intake comes from high-quality proteins (such as fish and legumes).
150 minutes of moderate-intensity aerobic exercise per week (such as brisk walking or swimming) combined with resistance training can effectively reduce liver fat content. Studies show that exercise plans combined with intermittent fasting can enhance insulin sensitivity by over 20%. Exercise intensity should be adjusted based on liver function, and patients with severe cirrhosis should avoid excessive energy expenditure training.
Controlling weight to a BMI < 24 is a key strategy, with weight loss of 7-10% proven to significantly improve liver fat accumulation. Patients with concurrent diabetes should keep HbA1c below 6.5%, and those with hyperlipidemia should reduce low-density lipoprotein to <100 mg/dL. Alcohol cessation is the first-line treatment for alcoholic fatty liver patients, requiring complete abstinence from alcohol consumption.
Gene therapy and liver-targeted drugs are current research hotspots, with techniques using nanoparticle carriers to deliver siRNA to inhibit liver fat synthesis pathways in clinical trial stages. Mesenchymal stem cell transplantation attempts to repair liver fibrotic tissue, but long-term safety remains to be observed.
Artificial intelligence diagnostic systems can assess liver fat ratios in real-time, combined with wearable devices to track metabolic indicators, potentially forming a personalized treatment platform in the future. Genetic profiling analysis will assist in predicting treatment responses, such as patients with PPARG gene polymorphisms responding better to specific medications.
Immediate medical attention should be sought when experiencing unexplained fatigue, right upper abdominal bloating or pain, or jaundice. If liver function tests show an AST/ALT ratio > 2, or ultrasound shows severe fatty liver (S2-S3 level), referral to a gastroenterologist or hepatobiliary specialist for further evaluation is necessary. Patients with concurrent type III hyperlipidemia or metabolic syndrome should have liver ultrasounds followed up every 6 months.
If liver fat content does not improve after 6-12 months of treatment, or symptoms of portal hypertension (such as esophageal varices) occur, evaluation of the treatment plan by a liver specialist is required. During pharmacological treatment, regular monitoring of liver enzymes and kidney function is necessary, especially for those using vitamin E for more than 6 months, who should be aware of the risk of fat-soluble vitamin metabolism abnormalities.
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