An Unexpected Cause of Non-alcoholic Fatty Liver Disease

An Unexpected Cause of Non-alcoholic Fatty Liver Disease

InterClinical eNews February 2018, Issue 77

In this month’s issue, we look at recent research examining what might cause non-alcoholic fatty liver disease and in patients with none of the usual risk factors.

Non-Alcoholic Fatty Liver Disease (NAFLD) is a serious condition which is on the increase and has now become the most common liver disease in industrialised countries. A diagnosis of NAFLD involves a tissue biopsy or medical imaging. The factors leading to the development of NAFLD are multifactorial, such as metabolic, genetic, infectious agents, exposure to certain drugs and chemicals.

More recently, dietary copper deficiency has also been implicated in NAFLD’s development. Copper is an essential trace element which is an integral component in several antiinflammatory hepatic enzymes including copper-zinc superoxide dismutase, metallopeptidase and metallothioneins.

The results showed low hepatic copper was independently and negatively associated with moderate to severe steatosis but only in patients without MetS. P <0.001.

Widely accepted predisposing factors such as high blood pressure, high blood sugar, high serum triglycerides and low levels of high-density lipoprotein; collectively called Metabolic Syndrome. To investigate the role of other possible agents, this large-scale study comprising 174 adults caucasian adults sought to evaluate the role of hepatic copper, and a genetic polymorphism (PNPLA3) in non-alcoholic fatty liver disease (NAFLD) in patients with or without Metabolic Syndrome (MetS).  The participants underwent liver biopsy and the percentage steatosis was calculated. Hepatic copper levels were also measured by spectroscopy.In recent years there has been a substantial number of people presenting with NAFLD symptoms Similarly liver fibrosis was significantly more common in NAFLD participants with low copper but these experimental results show that pathways other
MetS P <0. 001 The mechanism by which low copper leads to the development of steatosis is currently not well understood. However, some clues are emerging as patients with low copper tend to have elevated iron concentrations, a higher prevalence of siderosis and decreased levels of the hepatic iron transporter hepatic ferroportin mRNA. Low hepatic copper and the genetic polymorphism (PNPLA3) are emerging as independent contenders for the development of NAFLD, especially in those with normal body weight and without any signs of metabolic syndrome. 


  1. Stättermayer AF, Traussnigg S, Aigner E, Kienbacher C, Huber-Schönauer U, Steindl-Munda P, Stadlmayr A, Wrba F, Trauner M, Datz C, Ferenci P. Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome. Journal of Trace Elements in Medicine and Biology. 2017;39:100-7.

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