There is insufficient evidence to claim that high consumption of fructose, when part of isocaloric diet (no weight gain), is a risk factor for non-alcoholic fatty liver disease (NAFLD).
Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease (PubMed, 2017):
...the available evidence from human epidemiological and
interventional studies does not support the hypothesis that
fructose, when consumed in isocaloric amounts, causes more liver fat
accumulation than other energy-dense nutrients. The observed
prosteatotic effect of fructose in hypercaloric trials is likely
confounded by associated weight gain...
Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials (PubMed, 2014):
Isocaloric exchange of fructose for other carbohydrates does not
induce NAFLD changes in healthy participants.
Consumption of fruits, if part of isocaloric diet, is also not likely associated with NAFLD.
No association between fruits or vegetables and non-alcoholic fatty liver disease in middle-aged men and women (PubMed, 2019):
No obesity-independent association was found between fruit or
vegetable intake and NAFLD.
The main source of dietary fructose are probably soft drinks, not fruits, anyway:
- Popular soft drinks can contain 60-70 g fructose per liter (ScienceDirect, Fig. 2).
- Four apples (150 g each) contain 36 g fructose, which is more than in most other fruits (USDA.gov).
And finally, even if there is abundant evidence that fructose stimulates lipogenesis in the liver, this does not automatically mean that it stimulates the development of NAFLD (according to the first source above).