Several studies have shown that NAFLD is the main cause of chronic liver disease [25
]. In China, the prevalence of NAFLD varied widely due to differences in occupation, age, gender, life-style and regions studied [26
]. Previous studies had reported the prevalence of NAFLD in the general population of central China, Chengdu (Southwest China), Guangdong (South China) and Shanghai (East China) as 24.5%, 12.5%, 17% and 15% respectively [27
]. Regional variations within China can be striking. Due to the difficulty of carrying out large scale population survey, the true prevalence of the general population in China is still absent. In this study, we investigated the prevalence of NAFLD in employees in Shanghai to evaluate the trends of NAFLD prevalence rates. Our study reveals that the present prevalence of NAFLD in Shanghai is 38.17%, much higher than the previous study. Our study also investigated the prevalence of the components of metabolic syndrome. The prevalence of obesity, hypertension, dyslipidemia and T2DM are 30.63%, 29.82%, 28.59% and 11.4% respectively. Therefore, the difference of the present and previous prevalence could be attributed to the increasing prevalence of obesity, hypertension, insulin resistance and T2DM.
Our study investigated the employees in an age range of 18–64 years old. The study confirmed that the prevalence of NAFLD increases with increasing age and the peak prevalence of NAFLD was between 50–65 years old. However, it is difficult to generalize our results to the very old as our subjects were mainly the ‘younger old’ with few being aged
65 years. Further studies focusing specifically on the ‘old’ with NAFLD are needed.
Gender difference in the relationship between metabolic risk factors and NAFLD was another important finding in this study. A study conducted in a Korean population reported that the prevalence of NAFLD was 35% for men and 16% for women [30
]. Our study revealed that the prevalence of NAFLD was estimated to be 47.88% for men and 23.28% for women, higher than Koreans. The data of higher prevalence of NAFLD among men compared to women was also supported from studies in USA, Japan and India [31
]. This gender difference of prevalence maybe attributed to higher prevalence of metabolic syndrome in men [31
]. The national difference in prevalence may be owing to ethnicity and lifestyle differences. In this study, the average age in the male NAFLD group was younger than the female group. In the same age group, the prevalence of NAFLD in men was higher than women. Logistic regression analysis of risk factors for NAFLD revealed that high TG level was the most relevant factor for NAFLD in men, while obesity was the most strongly associated factor for NAFLD in women (obesity defined by BMI
). These age and gender differences may be due to differences in prevalence of obesity and life-style-related disease.
All these differences above can be explained by genetic predisposition. A genetic underpinning for NAFLD is suggested by a number of studies [10
]. In 2008, Romeo et al. conducted the first genome wide association study and reported the strongest genetic signal for the presence of fatty liver (PNPLA3
, patatin-like phospholipase domain containing 3; rs738409). It was reported that PNPLA3
and four additional genetic variants had a modest role for lipid metabolism. The PNPLA3
gene is responsible for the difference in prevalence of fatty liver disease between ethnic groups. It could also be responsible for a lower prevalence of steatosis in males [34
]. Apart from the PNPLA3
gene, many other genes can also influence the development of obesity and NAFLD via affecting lipid metabolism, cytokines, fibrosis mediators and oxidative stress [10
]. Genetic factors shed a light in the identification of individuals at risk to develop NAFLD and its progression.
Many studies have proposed that the risk factors for NAFLD included a high fat diet, a sedentary lifestyle, insulin resistance, metabolic syndrome and its components (obesity, hypertension, dyslipidemia and T2DM) [2
]. In our study, the ROC curves revealed that BMI, WC, weight-to-height ratio, BP, FPG, TC, TG, LDL, HDL and UA have diagnostic value for NAFLD. In western countries, visceral obesity had been shown to have a more important role in the pathogenensis of NAFLD than overall obesity. So WC has been a well-known surrogate marker of abdominal fat accumulation. But our studies revealed that BMI was superior to WC, and BMI is a better index for diagnosing NAFLD. Recently, many studies recommended that weight-to-height was an index not affected by height, it may be a good index for detecting NAFLD. But our study found that there was no significant statistical difference in the AUCs of weight-to-height ratio and WC, suggesting that waist-to-height ratio and WC has the same value for detecting NAFLD.
Recent studies have reported that serum uric acid levels were associated with NAFLD [38
].The most significant finding of this study is that UA has a more diagnostic value for NAFLD. Our study found that there is no significant statistical difference in the AUCs of FPG and UA in males. UA is not inferior to FPG in diagnosing NAFLD. There are no significant statistical differences in the AUCs of UA and TC, LDL, BG, DBP in females. UA is not inferior to TC, LDL, BG and DBP in diagnosing NAFLD.
Our logistic regression analysis revealed that each component of metabolic syndrome was independently associated with NAFLD. Obesity, central obesity, BP
130/85mmHg and/or hypertension, dyslipidemia, high uric acid and FPG
5.6mmol/L and/or T2DM can increase the risk of NAFLD by 1.5
3.8 times. Previous studies had reported that obesity was the strongest associated factor after adjusting for age, gender and other metabolic factors [30
]. But we found that obesity was the most relevant factor in females, which can increase the risk of NAFLD by 3.8 times, while it is hypertriglyceridemia in males, which can increase the risk of NAFLD by 3.8 times. In males, obesity is secondary to hypertriglyceridemia, with 3.3 times risk increase for NAFLD.
The present study does have some limitations. First, we tried our best to exclude subjects with a history of habitual alcohol consumption in this study. However, since the limit of excessive alcohol use probably needs to be adjusted according to the size of body and gender, the exact amount of alcohol consumed and its alcoholic content were difficult to assess. Second, although histopathological findings remain the gold standard for diagnosing NAFLD, they cannot be applied to a large-scale population. Abdominal US is non-invasive, easily undertaken and has a sensitivity ranging from 60% to 94% and a specificity from 84% to 95% in detecting the presence of fatty liver. If the hepatic steatosis reaches 33%, sensitivity approaches 100% [18
]. So we used abdominal US to diagnose fatty liver. But when the infiltration is of less than 30% of the hepatic content, it is difficult to detect the presence of fatty liver. Finally, other confounders such as physical activity should also be considered. Further studies are required to adjust for these possibly distorted associations and to validate these findings to other populations.