ABSTRACT
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is characterized by hypertriglyceridemia, increased low-density lipoprotein cholesterol levels, and reduced high-density lipoprotein cholesterol (HDL-C) particles. Previous studies have shown that the total cholesterol to high-density lipoprotein cholesterol ratio (TC/HDL-C) was superior to other lipid metabolism biomarkers for predicting NAFLD risk and could be a new indicator of NAFLD. However, the association between TC/HDL-C and NAFLD in patients with hepatitis B virus (HBV) has not yet been determined. AIM: To investigate the association between TC/HDL-C and NAFLD in a population with chronic hepatitis B (CHB). METHODS: In this study, 183 HBV-infected patients were enrolled. All participants underwent blood chemistry examinations and abdominal ultrasound. Univariate and multivariate logistic regression models, curve fitting analysis, and threshold calculation were used to assess the relationship between TC/HDL-C and NAFLD. RESULTS: The overall prevalence of NAFLD was 17.49% (n = 32) in the 183 CHB participants. The TC/HDL-C of non-NAFLD and NAFLD patients were 3.83 ± 0.75 and 4.44 ± 0.77, respectively (P < 0.01). Logistic regression analysis showed that TC/HDL-C was not associated with NAFLD after adjusting for other pertinent clinical variables. However, at an optimal cutoff point of 4.9, a non-linear correlation between TC/HDL-C and NAFLD was detected. The effect size of the left and right sides of the inflection point were 5.4 (95% confidence interval: 2.3-12.6, P < 0.01) and 0.5 (95% confidence interval: 0.1-2.2, P = 0.39), respectively. On the left side of the inflection point, TC/HDL-C was positively associated with NAFLD. However, no significant association was observed on the right side of the inflection point. CONCLUSION: This study demonstrated a non-linear correlation between TC/HDL-C and NAFLD in a population with CHB. TC/HDL-C was positively associated with NAFLD when TC/HDL-C was less than 4.9 but not when TC/HDL-C was more than 4.9.
ABSTRACT
OBJECTIVE: To observe the effect of berberine on uncoupling protein-2 (UCP2) mRNA and protein expressions in the hepatic tissue of non-alcoholic fatty liver disease (NAFLD) in rats, and to explore the molecular mechanism. METHODS: To establish the NAFLD rat model; the rats were fed by high fat forage and were randomly divided into four groups: normal group, model group, berberine high-dose group (324 mg/kg), and berberine low-dose group (162 mg/kg). After treatment for 12 weeks, the expression of UCP2 mRNA in the liver tissue was analyzed by semiquantitative reverse transcription polymerase chain reaction (RT-RTPCR). The expression level of UCP2 protein in the liver tissue was examined by immunohistochemistry. Total PCR). cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) contents in blood serum, and TG and TC contents in the liver were detected by an automatic biochemical analyzer. The other is to observe the axungia degree of the liver. RESULTS: The expression of UCP2 mRNA and positive cell numbers in the liver tissue were dramatically increased in the model group (P<0.01). Lipid in the serum and hepatic tissues increased significantly, and the liver was fatty. But in the treatment groups, the expression levels of mRNA and UCP2 proteins were significantly down-regulated (P<0.01). Liver steatosis was improved. CONCLUSIONS: Berberine can down-regulate the expression levels of UCP2 mRNA and UCP2 proteins of hepatic tissue in NAFLD rats. It can promote the recovery of hepatocyte steatosis and improve lipid metabolism disorder in NAFLD rats. Berberine shows a potential therapeutic effect on NAFLD.
