Although the relationship between these FL related indexes (SBP, DBP, TC, TG, LDL, FBG, ALT, AST, WC, WHR, WHtR, BMI, AVI, AIP, TyG and ALT/AST) and FL were analyzed separately in many articles, few articles put them together to evaluate. In this cross-sectional survey, we comprehensively evaluated the predictive ability and cutoff value of anthropometric and metabolic indices, including SBP, DBP, FBG, TC, TG, LDL, ALT, AST, WC, WHR, WHtR, BMI, AVI, AIP, TyG and ALT/AST, in identifying FL among adults and found that the ORs in females increased more per quartiles than that in males. WHtR had the greatest AUC regardless of gender. Furthermore, WC and AVI had the greatest AUC in 20–40 years (AUC = 0.96) of females, while TyG had the greatest AUC in 40- years (AUC = 0.80) of females.
The prevalence of FL might be influenced by gender and age[3, 4, 8]. In our study, we found that men had a similar prevalence of FL regardless of age, whereas in women the prevalence of FL increased steadily with age. As we all know that sex hormones play a central role in predisposing individuals to metabolic status. Loss of estrogen after menopause leads to extensive changes in the metabolic system, including an increase in visceral adiposity. Although FL is primarily a male disease, the alteration in sex hormone levels, specifically reduced estrogens and increased androgens during and after menopause, is an important factor in the emergence of FL for female subjects[30, 31]. A study of Japanese women showed aging is a risk factor for FL in premenopausal women, independently from weight gain or influence of metabolic syndrome.
The association of obesity with FL has been established in multiple previous studies[11, 15, 33, 34]. Epidemiological studies propose a causative link between obesity and progressive liver disease in individuals[15, 34]. Obesity has been linked not only to the initial stages of the disease, but also to its severity. The pathophysiology and clinical studies have shown that the progression of FL results from an imbalance between lipid uptake and lipid disposal and eventually causes oxidative stress and hepatocyte injury. Obesity can be expressed in clinical practice by several methods, including anthropometric and metabolic ways. Some studies thought that the visceral adiposity was the main adipose depot responsible for FL and was associated with FL in a dose-dependent manner in a cohort study. WC, WHR, WHtR and BMI have been proved and used in many clinical trials as an indicator for the severity of fatty liver disease[19, 22]. AVI is used to assess general volume, and it has been highly associated with dysfunction of glucose metabolism. Researches found that there were concordances between increased AIP and the incidence of FL[17, 18]. TyG are often used to explore the relationship between insulin resistance and excessive visceral fat accumulation[38, 39]. Additionally, accumulating evidence strongly suggests that advanced blood lipids, blood pressure and blood sugar could also lead to more severe histological changes and poorer clinical outcomes[14, 22, 40]. Once FL is established, insulin resistance can promote the progression to the more severe state of liver endangerment like non-alcoholic steatohepatitis.
In our study, we found differences of these related indexes between FL and non-FL stratified by the gender. We firstly demonstrated that the ORs in females increased more per quartiles than that in males. This may be explained by hormone changes in age. Testosterone has been shown to increase their risk of FL in females with polycystic ovary syndrome, independently from obesity and insulin resistance. The study by Park et al. expands upon existing data by highlighting the association of testosterone and FL even among women without “high” testosterone levels. A research in Development in Young Adults cohort found that increasing levels of free testosterone in premenopausal women were associated with prevalent NAFLD in midlife, including women without androgen excess.
Our results further revealed that WHtR had the strongest association and diagnostic ability (cut-off points, 0.505 in men and 0.525 in women) with FL after considering the influence of gender, which is consistent with the research by Nima Motamed et al. who calculated cut-off points for WHtR (0.533 in men and 0.58 in women). The subtle differences between the two studies may be owing to difference between Chinese and Iranian. Our findings is in contrast with the study by Zheng et al., who reported the ability of WHtR for predicting FL was weaker than WHR, it should be mentioned that their research may be more useful in the prediction of FL for males due to the high proportion of males and low number of study population . Additionally, we found an age-specific effects of these marker for predicting FL. As we all know, diabetes is one of the strongest risk factors for FL, the increasing prevalence of diabetes along with age especially in female subjects s[12, 46] may explain the result that WC and AVI had the greatest AUC in 20–40 years, while TyG had the greatest AUC in 40- year.
This study evaluated the predictive ability and cutoff value of anthropometric and metabolic indices. However, there are still some limitations. Firstly, our findings are based on a cross-sectional study, a large-scale cohort study is still necessary to build the definite causal relationship between these indices and FL. Secondly, the data of other confounders, such as, smoking and drinking status and exercise, were not included in this analysis because of the information default.