Letter to the editor: Adipose lipolysis is important for ethanol to induce fatty liver in the NIAAA murine model of chronic and binge ethanol feeding

To the editor, We followed with interest the report by Mathur et al.1 on adipose lipolysis in mediating ethanol‐induced hepatic steatosis and lipid peroxidation, eventually leading to fatty liver. There are some disputes and defects in the experimental model. Firstly, the baseline of mice was different (male aged 8–10 weeks and female aged 10–12 weeks), and the alanine transaminase (ALT) and aspartate transaminase in the adipose‐specific Comparative Gene Identification‐58 knockout group were significantly higher than those in the wild‐type group. Meanwhile, some confounding factors affecting alcoholic fatty liver disease (AFLD) and hepatic steatosis were not included, such as initial hormone levels, body mass index, and primary disease.2 No clear statement about these factors between the groups was shown, and the samples are pretty small. Secondly, the feeding pattern in the article is unsuitable. In Figure S1A of Mathur et al., the feeding doses of the experimental group and the control group were different. Previous studies have shown that different feeding doses (50 g vs. 65 g) within a week can lead to differences in ALT, alkaline phosphatase, and insulin‐like growth factor‐1.3 In Figure S1C, almost all mice have significant weight loss after 15 days of feeding, regardless of feeding pattern. In a standard National Institute on Alcohol Abuse and Alcoholism model, no significant difference was found in the weight of mice through the trial.4 In addition, a recent study showed that an inadequate diet could significantly lead to fatty liver.5 This study is susceptible to selection bias because various factors may lead to fatty liver in mice. Thirdly, the diagnostic criteria for fatty liver are not given in this article. This study should provide a quantitative analysis of pathological hepatocyte sections for diagnosing fatty liver. In conclusion, this study provides a new reference for adipose lipolysis playing a vital role in fatty liver, but AFLD may not be relevant.