Increased levels of obesity are driving an epidemic of non-alcoholic fatty liver disease. Understanding, diagnosing and treating this progressive condition are now priorities.
Calories not alcohol
An advanced stage of non-alcoholic fatty liver disease (NAFLD) was first described in 1980, confirming that liver disease characterized by an accumulation of fat can develop in people who do not consume excess alcohol1. Associated with obesity and type 2 diabetes, NAFLD is set to become the most common cause of serious liver disease in many nations.
Age, gender and genetics all contribute to a person’s risk of developing NAFLD and NASH. But the main risk factors are obesity and diabetes, as well as other features of metabolic syndrome, including high blood pressure and insulin resistance.
The link between obesity, its complications and NAFLD is strong.
Diabetes and insulin resistance
In healthy people, insulin inhibits the breakdown and release of fat by fat cells (adipocytes).
In people with insulin resistance, fat is secreted into the bloodstream, from where it is taken up by hepatocytes.
To determine the extent of NAFLD and associated fibrosis, and to monitor patients’ responses to treatment — without using an invasive liver biopsy — biomarker discovery and advances in imaging technology are needed.
In the blood
Although current blood tests for liver disease can help to assess the severity of NAFLD, researchers are seeking new biomarkers with concentrations that reliably correlate with disease activity.
Diagnostic tools that use ultrasound technology can help to assess the health of the liver, but the fine resolution and sensitivity of such techniques needs improvement.
The cornerstones of NAFLD treatment are weight loss and increased amounts of exercise, but maintaining these lifestyle changes can be hard. NASH is now considered to be a serious condition that requires the development of targeted drugs. As a result, hundreds of trials of potential treatment strategies are under way.
1. Ludwig, J., Viggiano, T. R., McGill, D. B. & Oh, B. J. Mayo Clin. Proc. 55, 434–438 (1980).
2. Younossi, Z. M. et al. Hepatology 64, 73–84 (2016).
3. Rinella, M. E. JAMA 313, 2263–2273 (2015).
4. Younossi, Z. M. et al. Clin. Gastroenterol. Hepatol. 9, 524–530 (2011).
5. Lazo, M. et al. Am. J. Epidemiol. 178, 38–45 (2013).
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