Non-alcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance, with a fundamental characteristic being a reduced responsiveness to insulin i.e. reduced insulin sensitivity. There are numerous factors that contribute to fat build up in the liver which will be discussed in detail below. Fatty liver may cause inflammation which may therefore scar the liver and result in liver failure.

NAFLD is used to describe fatty liver disease in people without a history of excessive alcohol intake. The accumulation of fat leads to fat toxicity, which promotes inflammation and insulin resistance in the liver. Under normal conditions, the pancreas releases insulin after a meal. Thus, insulin regulates the breakdown of glucose, as well as being vital for the synthesis and breakdown of fat in cells. 

There are a number of mechanisms that cause fatty liver including increased intake of dietary fats, increased fat production (from the breakdown of excess carbohydrates) and the increased amount of free fatty acids (i.e. the building block of fat in our bodies and food we eat). Interestingly, the increased free fatty acids interact with insulin signalling, therefore contributing to the insulin resistance. Therefore, in the presence of insulin resistance, the liver may produce triglycerides (i.e. type of fat) which also contributes to the development of NAFLD. 

Inflammation also contributes to insulin resistance, with inflammation markers being expressed in fat tissue and the liver. Obesity (which is a state of chronic low-grade inflammation) is a risk factor for insulin resistance and NAFLD. Therefore, obesity results in a decreased sensitivity to insulin which renders insulin inefficient. In addition, leptin (which is a hormone found in fat tissue) has the role of worsening insulin resistance as higher leptin levels cause it to be released from fat cells. Hence, there is a direct correlation between higher leptin levels and severity of NAFLD. 

The processes of insulin resistance and NAFLD are summarised as follows: 

  • Fat cells release a hormone (known as adiponectin) which allows your cells to respond to insulin. Thus, people with NAFLD have lower levels of adiponectin, which means they are not as equipped to respond to insulin compared to those without NAFLD. 
  • The formation of fatty acids, which is activated by a high availability of carbohydrates. Excess fatty acids are released into the bloodstream and are deposited into the liver rather than fat tissue.
  • The inflammation of fat tissue is associated with insulin resistance. Thus, inflammation markers are higher in people with NAFLD.

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Further Reading

Written by 
Mary-Anne Chamoun
Mary-Anne is an Accredited Practising Dietitian and Accredited Nutritionist who has been working in a clinical setting since 2007. She has a particular interest in managing diabetes, malnutrition, IBS, inflammatory bowel disease, and weight loss.