No pharmacologic therapies have yet been approved for the treatment of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), its progressive form. Instead, NAFLD is currently managed by lifestyle interventions, including dietary modifications and physical exercise. Despite this, evidence regarding the effect of exercise on NAFLD-associated histological endpoints is lacking.
In this video Prof. Sven Francque explores that NAFLD is prevalent in patients with cardiovascular disease, but this does not prove bidirectional causality. Vascular mechanisms contribute to NASH pathogenesis and drugs used in CVD management show some benefit on NAFLD.
A 2022 study by Ajmera and colleagues examined the prevalence of non-alcoholic fatty liver disease (NAFLD), advanced fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) in older patients with type 2 diabetes (T2D). The strong association between T2D, NAFLD, and its progressive form non-alcoholic steatohepatitis (NASH) has been extensively underscored by recent literature.
The circadian clock controls rhythms responsible for regulating bodily functions, e.g., appropriate eating times. When this clock becomes disrupted due to factors such as irregular daily eating patterns or weekly schedules, it instead promotes lipid dysregulation, oxidative stress, and inflammation.
The circadian clock controls rhythms responsible for regulating bodily functions, e.g., appropriate eating times. When this clock becomes disrupted due to factors such as irregular daily eating patterns or weekly schedules, it instead promotes lipid dysregulation, oxidative stress, and inflammation.
The circadian clock controls rhythms responsible for regulating bodily functions, e.g., appropriate eating times. When this clock becomes disrupted due to factors such as irregular daily eating patterns or weekly schedules, it instead promotes lipid dysregulation, oxidative stress, and inflammation.
Currently, the most effective treatment for non-alcoholic fatty liver disease (NAFLD) is diet and exercise. Weight loss of 5% achieved through lifestyle interventions has been associated with the reversal of steatosis, and a 10% weight reduction has been linked to the reversal of fibrosis. Physical activity (PA) has been hypothesised to reduce the accumulation of intrahepatic triglycerides contributing to NAFLD progression.
Research in recent years has documented the rise of quantitative ultrasound-based examinations (qnUS) for the assessment of liver steatosis. qnUS of interest include continuous attenuation parameters (CAP), backscatter coefficients, and ultrasound envelope statistic parametric imaging. Despite the clear financial and patient-centric benefits of such non-invasive tools, their reliability in defining both the presence and degree of liver steatosis remains unclear.
Dysfunctional visceral adipose tissue is one of the major drivers and determinants of non-alcoholic fatty liver disease (NAFLD). Due to an inability to store excess energy in adipose tissue compartments, the body resorts to storing it in ectopic fat compartments. Compared with lean individuals, people who are overweight or obese are thus at a higher risk of developing NAFLD.
Dr. Laurent Castera (France) discusses how healthcare professionals can integrate non-alcoholic steatohepatitis (NASH) assessment and management into the care of diabetic patients in order to provide a holistic approach for the patient in order for improved patient outcomes.
Patients and physicians have to know that NASH increases the risk to develop cancers. Specific surveillance has to be implemented when indicated. Hepatocellular carcinoma is rare in patients with NASH without advanced fibrosis, but seems to occur not rarely when the liver is not yet cirrhotic. Some molecular mechanisms seem specific to NASH-related HCC. The management is similar to HCC with other underlying liver disease. Patients with NASH-related HCC may respond less to immuno-oncology.
The best treatment for NASH still remains as caloric intake reduction, weight loss, exercise and no heavy alcohol consumption, but these are merely lifestyle changes. There appears to be a fibrosis regression over time following bariatric surgery in patients with severe obesity and NASH. Liver histologic improvement endpoints are likely to predict clinical benefits. NAFLD liver fibrosis is a risk factor for adverse outcomes. Improvement in the NASH fibrosis stage was associated with lower risk of liver-related outcomes. Multifactorial metabolic milieu of NASH warrants potential combination therapy targeting many pathways.