Non-Alcoholic Steatohepatitis (NASH) – Metabolic Contributors and Therapeutic Targets

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Magdalene K Montgomery

The University of Melbourne

Karine Clément

Sorbonne Universités

Shingo Kajimura

Beth Israel Deaconess Medical Center, Harvard Medical School

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This Research Topic focuses on the themes of the 2020 Keystone Symposium Obesity and NAFLD: Mechanisms and Therapeutics.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver condition in developed countries and a?ects 20-40% of the general population. A major risk factor for NAFLD is obesity, which now a?ects 25-30% of individuals worldwide. NAFLD involves a spectrum of liver diseases that range from simple steatosis to its progressive form, non-alcoholic steatohepatitis (NASH). Around 25-30% of patients with NAFLD have NASH, which may lead to the development of cirrhosis and its complications, such as portal hypertensive bleeding, hepatocellular carcinoma, and hepatic decompensation.

One of the ?rst metabolic defects that occurs during the development of NAFLD is hepatic lipid accumulation (steatosis), with this 'lipotoxic' state further driving in?ammation and ?brosis within the liver. Therefore, tackling such early metabolic defects (ie. inhibiting hepatic steatosis) is likely to have the capacity to prevent NASH development. However, despite NAFLD being one of the most common metabolic diseases in developed countries, there are currently no approved therapies for NASH and no therapies that directly target lipid accumulation and ?brosis.

In addition to obesity, NAFLD increases the risk of developing type 2 diabetes (T2D) by 3-5 fold, which is associated with increased severity of micro- and macrovascular complications in T2D patients with NAFLD compared to those without a fatty liver. On the other hand, the presence of T2D significantly increases the risk of developing NAFLD, which highlights the bi-directional nature of the metabolic impact of T2D and NAFLD.

This Research Topic will focus on understanding NASH development, the prevalence of metabolic co-morbidities in NASH patients (with a focus on obesity and T2D), and therapeutic strategies for hepatic steatosis, NASH, and fibrosis.

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Editors

Magdalene K Montgomery

The University of Melbourne

Karine Clément

Sorbonne Universités

Shingo Kajimura

Beth Israel Deaconess Medical Center, Harvard Medical School

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Published In

Frontiers in Endocrinology

Obesity

Frontiers in Public Health

Obesity

Frontiers in Nutrition

Obesity

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