Abstract Background Acrylamide (AA) is a toxicant to humans, but the association between AA exposure and the risk of non-alcoholic fatty liver disease (NAFLD) remains unclear. In this study, our objective is to examine the cross-sectional association between AA exposure and the risk of NAFLD in American adults. Methods A total of 3234 individuals who took part in the National Health and Nutrition Examination Survey (NHANES) 2003–2006 and 2013–2016 were enrolled in the study. NAFLD was diagnosed by the U.S. Fatty Liver Index. Multivariable logistic regression models were applied to estimate the association between AA and NAFLD in the whole group and the non-smoking group. Results We discovered that in the whole group, serum hemoglobin adducts of AA (HbAA) were negatively associated with the prevalence of NAFLD after adjustment for various covariables ( P for trend < 0.001). Compared with individuals in the lowest HbAA quartiles, the odds ratios (ORs) with 95% confidence intervals (CIs) in the highest HbAA quartiles were 0.61 (0.46–0.81) and 0.57 (0.36–0.88) in the whole group and the non-smoking group, respectively. In contrast, HbGA/HbAA showed a significantly positive correlation with the prevalence of NAFLD in both groups ( P for trend < 0.001). In addition, HbGA was not significantly associated with NAFLD in the whole group or the non-smoking group. Conclusions HbAA is negatively associated with NAFLD whereas HbGA/HbAA is positively associated with NAFLD in adults in the U.S. Further studies are needed to clarify these relationships.
Abstract Serum complement C3 levels are closely associated with obesity and related metabolic disorders. This study aimed to investigate the association between serum complement C3 levels with non-alcoholic fatty liver disease (NAFLD). A cross-sectional study was performed among adults who took their annual health examinations at Zhenhai Lianhua Hospital, Ningbo, China during 2014. We included 7540 participants (5069 men and 2471 women) in this study. NAFLD patients had higher serum complement C3 levels ( P < 0.001) and these levels were positively associated with both NAFLD prevalence and severity ( P < 0.001). The above association remains true among lean and metabolic syndrome-free participants. Multivariable regression analysis showed that serum complement C3 was independently associated with risk for NAFLD (OR = 5.231; 95% CI: 3.169–8.635). Serum complement C3 level is positively associated with prevalence and severity of NAFLD and this association is independent of obesity and metabolic syndrome.
Autoimmune pancreatitis (AIP) is a special type of chronic pancreatitis, which may be misdiagnosed as pancreatic carcinoma. This study aims to verify new biomarkers for AIP and propose a serological pattern to differentiate AIP from pancreatic adenocarcinoma with routinely performed tests. In this study, data of serum samples were collected and compared between 25 patients with AIP and 100 patients with pancreatic carcinoma. Receiver operating characteristic analysis and logistic regression was performed to evaluate the diagnostic effect of serum parameters in differentiating AIP from pancreatic carcinoma alone or in combination. Among several serum markers observed in the two groups, carbohydrate antigen 19–9 (Ca19-9), globulin, eosinophils and hemoglobin were selected as the independent markers. Serum levels of Globulin, Eosinophil percentage in AIP group were significantly higher than in pancreatic cancer group (P<0.05), while hemoglobin and tumor marker CA19-9 levels were lower (P <0.05). The combination of these markers identified patients with AIP with 92% sensitivity and 79% specificity, which indicated relatively high diagnostic value. Elevated serum eosinophils, globulin, together with decreased hemoglobin level can be used as a preoperative indicator for AIP and can help to initiate diagnosis of AIP in time.
Caveolin1 (CAV1) is involved in lipid homeostasis and endocytosis, but little is known about the significance of CAV1 in the pathogenesis and development of nonalcoholic fatty liver disease (NAFLD). This study aimed to determine the role of CAV1 in NAFLD.Expression of CAV1 in the in vitro and in vivo models of NAFLD was analyzed. The effects of CAV1 knockdown or overexpression on free fatty acid (FFA)-induced lipid accumulation in L02 cells and AML12 cells were determined. CAV1 knockout (CAV1-KO) mice and their wild-type (WT) littermates were subjected to a high fat diet (HFD) for 4 weeks, and the functional consequences of losing the CAV1 gene and its subsequent molecular mechanisms were also examined.Noticeably, CAV1 expression was markedly reduced in NAFLD. CAV1 knockdown led to the aggravation of steatosis that was induced by FFA in both L02 cells and AML12 cells, while CAV1 overexpression markedly attenuated lipid accumulation in the cells. Consistent with CAV1 repression in the livers of HFD-induced mice, the CAV1-KO mice exhibited more severe hepatic steatosis upon HFD intake. In addition, increased cholesterol levels and elevated transaminases were detected in the plasma of CAV1-KO mice. The protein expression of SREBP1, a key gene involved in lipogenesis, was augmented following CAV1 suppression in FFA-treated hepatocytes and in the livers of HFD-fed CAV1-KO mice.CAV1 serves as an important protective factor in the development of NAFLD by modulating lipid metabolism gene expression.
The role of fatty acids (FAs) in primary prevention of coronary artery disease (CAD) is highly debated, and the modification effect by genetic risk profiles remains unclear. Here, we report the prospective associations of circulating FAs and genetic predisposition with CAD development in 101,367 U.K. Biobank participants. A total of 3719 CAD cases occurred during a mean follow-up of 11.5 years. Plasma monounsaturated FAs (MUFAs) were positively associated with risk of CAD, whereas the risk was significantly lower with higher n-3 polyunsaturated FAs (PUFAs) and more reductions in risk were detected among TT carriers of rs174547. Furthermore, increased plasma saturated FAs (SFAs) and linoleic acid were related to a significant increase in CAD risk among participants with high genetic risk (genetic risk score > 90%). These findings suggest that individuals with high genetic risk need to reduce plasma SFAs levels for CAD prevention. Supplementation of n-3 PUFAs for CAD prevention may consider individuals' genetic makeup.
Growth hormone (GH) is an important regulator of metabolism and body composition. GH deficiency is associated with increased visceral body fat and other features of the metabolic syndrome. Here we performed a cross-sectional study to explore the association of GH levels with nonalcoholic fatty liver disease (NAFLD), which is considered to be the hepatic manifestation of the metabolic syndrome. A total of 1,667 subjects were diagnosed as NAFLD according the diagnostic criteria, and 5,479 subjects were defined as the controls. The subjects with NAFLD had significantly lower levels of serum GH than the controls. Those with low GH levels had a higher prevalence of NAFLD and the metabolic syndrome. A stepwise logistic regression analysis showed that GH levels were significantly associated with the risk factor for NAFLD (OR = 0.651, 95%CI = 0.574–0.738, P<0.001). Our results showed a significant association between lower serum GH levels and NAFLD.
The precise prevalence and risk factors for the development of nonalcoholic fatty liver disease (NAFLD) in nonobese adults remains unclear. The objective of this study was to investigate the prevalence of NAFLD and risk factors for its development in a nonobese Chinese population.We firstly investigated the prevalence and factors associated with the presence of NAFLD in nonobese (body mass index (BMI) <25 kg/m(2)) Chinese subjects via a cross-sectional study, and then analyzed the risk factors for the development of NAFLD via a subsequent prospective 5-year follow-up of the same population.A total of 6,905 nonobese subjects were enrolled in the cross-sectional study. Baseline evaluation revealed that the prevalence of NAFLD was 7.27%. A total of 5,562 subjects who were free of NAFLD at baseline completed the follow-up study, and 494 (8.88%) had developed NAFLD during the 5-year follow-up. Further analyses revealed that age, gender, BMI, waist circumference, triglyceride, high-density lipoprotein (HDL) cholesterol, serum uric acid, hemoglobin, and platelet count were independently associated with the presence and development of NAFLD.NAFLD is prevalent in the nonobese Chinese population, and a substantial proportion of subjects developed NAFLD over the 5-year follow-up period. Special attention should be paid to the factors associated with the presence and development of NAFLD in nonobese subjects, to improve prevention and management of NAFLD.
OBJECTIVE: This study explored the association between light-to-moderate alcohol consumption (LMAC) and risk of type 2 diabetes mellitus (T2DM) in individuals with nonalcoholic fatty liver disease (NAFLD). METHODS: A 9-year cohort study was performed among Chinese men who underwent their annual health checkups between 2009 and 2018. NAFLD was diagnosed based on abdominal ultrasound with exclusion of excess alcohol intake and other causes of liver disease. Logistic regression and Cox proportional regression analyses were applied to identify the risk of prevalent and incident T2DM. RESULTS: Of the 7,079 participants enrolled, 243 had T2DM at baseline and 630 developed T2DM during the 45,456 person-years follow-up. Both at the baseline and by the end of the follow-up, LMAC was associated with a decreased risk of prevalent T2DM in NAFLD-free participants but with a significantly increased risk in patients with NAFLD. LMAC was also associated with a decreased risk of incident T2DM in NAFLD-free participants. The adjusted hazard ratios (95% confidence interval) of incident T2DM were 0.224 (0.115–0.437) and 0.464 (0.303–0.710) for NAFLD-free light drinkers and NAFLD-free moderate drinkers, respectively. Nondrinking, light-drinking, and moderate-drinking patients with NAFLD all showed significantly increased risks of incident T2DM. Compared with NAFLD-free nondrinkers, the adjusted hazard ratios (95% confidence interval) of incident T2DM were 1.672 (1.336–2.092), 2.642 (1.958–3.565), and 2.687 (2.106–3.427) for nondrinking, light-drinking, and moderate-drinking patients with NAFLD, respectively. DISCUSSION: LMAC decreased the risks of prevalent and incident T2DM in NAFLD-free participants. LMAC, however, was associated with an increased risk of T2DM in patients with NAFLD (ClinicalTrials.gov number: NCT03847116).