Nonalcoholic fatty liver disease (NAFLD) is characterized as more than 5% of fat infiltration in the liver without alcohol consumption exceeding 30 g/day in men and 20 g/day in women, which is believed to be caused by abdominal obesity and insulin resistance. The underlying pathogenesis of nonalcoholic fatty liver disease (NAFLD) includes bodys inability to store excess energy in adipocytes; and considered as the hepatic manifestation of metabolic syndrome. Epidemiological surveys suggest that prevalence of NAFLD differs by ethnic group and diagnostic method, ranging from 15% to 70%.

However, the prevalence of NAFLD is exponentially rising due to increasing obesity and obesity-related comorbidities, worldwide. It is still known to be the most common cause of elevated liver enzymes in countries at different levels of development. The prevalence of NAFLD is estimated to be as high as 1 billion, worldwide, and NAFLD is the most prevalent cause of chronic liver disease in the United States, affecting 80 to 100 million individuals, with 25% of Nonalcoholic steatohepatitis (NASH) population. 

Several researches have examined the relationships of NAFLD with metabolic risk factors. High baseline insulin levels were related to a 1.2-fold increased risk of NAFLD after a period of 4 years, and the risk increased to 2.5-fold in patients who had both high insulin levels at baseline and 4 years later. Moreover, a study showed that patients who exercised more than five times a week reported a 14% lower risk for development of NAFLD in contrast to those who did not exercise at all.

Mounting evidences suggest that type 2 diabetes mellitus (T2DM) and NAFLD share insulin resistance as a common pathophysiological mechanism, and both diseases affects the development of one another. A study revealed that in a systematic review that NAFLD was present in 50% to 75% of T2DM patients, with variation according to ethnicity. Another survey suggested that NAFLD augments the risk of diabetes by 1.6 to 6.8 times in meta-analyses, with variation according to the adjusted other risk factors.

Moreover, T2DM can aggravate NAFLD by increasing the progression to NASH or fibrosis, while NAFLD causes the natural course of diabetic complications to worsen in T2DM patients. A study conducted in 129 subjects with biopsy-proven NAFLD with unknown glycemic status at baseline showed 78% patients with diabetes after 13.7 years of follow-up. Additionally, prominent insulin resistance was observed in participants with progressive fibrosis, suggesting that dysglycemia may promote progression to fibrosis.

Source: Endocrinol Metab (Seoul). 2019;34(3):226-233.