The inhibition of p38 and JNK improved the pathological state of liver lipid deposition and liver function to some extent, improved the degree of hepatic fibrosis, and reduced the apoptosis of hepatocytes in NAFLD rats.
Results revealed that miR-205 facilitated lipid accumulation by inhibiting NEU1 in NAFLD, suggesting that miR-205 might be a potential target for the therapeutic strategy for NAFLD.
The impact of uric acids on liver pathology, and the expression patterns of key molecules involved in the development of NAFLD, including silent information regulator 1 (SIRT1), nuclear factor kappa B subunit p65 (NF-κB p65), fork-head box class O-3a (FOXO3a), androgen receptor (AR), and xanthine oxidase (XO) were analysed.
In contrast, in livers with heterozygous <i>Hcfc1</i><sup>hepKO/+</sup> hepatocytes, HCF-1-positive hepatocytes replaced HCF-1-negative hepatocytes and revealed only mild-NAFL development.
The odds ratio for the incidence of NAFLD was 1.462 (1.029-2.077) for the group of people who sleep more than 8 h, 1.271 (1.001-1.615) for 7-8 h after adjusting for age, sex, BMI, SBP, DBP, TG, HDL, FDG, smoking, physical activity, daytime napping and night-time shifting (p < 0.01).
Collectively, ZHX2 protects hepatocytes from abnormal lipid deposition in NAFLD through transcriptional repression of LPL, which subsequently retards cell growth and NAFLD-HCC progression.
Taken together, the results of the present study demonstrated that SIRT1 deacetylated QKI 5, an RNA‑binding protein significantly affecting the synthesis of TG in the liver of the NAFLD mouse model.
SNPs in CYP2R1, DHCR7, vitamin D binding protein (GC), CYP27B1, and vitamin D receptor (VDR) were determined for 229 consecutive patients with biopsy-proven NAFLD.
Group VIA calcium-independent phospholipase A2 (iPla2β) is among modifier genes of non-alcoholic fatty liver disease which leads to non-alcoholic steatohepatitis (NASH).
After adjusted for age, gender, and body mass index, the risk for CHD in general population (OR = 1.857; 95% CI: 1.116-3.089; P = 0.017) and NAFLD patients was still significant (OR = 1.723; 95% CI: 1.033-2.873; P = 0.037).
The RRA integrated analysis determined 96 significant DEGs (50 up-regulated and 46 down-regulated) and the most significant gene aberrantly expressed in NAFLD was ENO3 (<i>P</i>-value = 7.17E-05), followed by CYP7A1 (<i>P</i>-value = 9.04E-05), and P4HA1 (<i>P</i>-value = 1.67E-04).
Here we demonstrate that G protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor corepressor (NCOR) and histone deacetylase 3 (HDAC3) complex, has a central role in these alterations and accelerates the progression of NAFLD towards non-alcoholic steatohepatitis (NASH).
Our results establish an essential role for the nuclear envelope-localized torsinA-LAP1 complex in hepatic VLDL secretion and suggest that the torsinA pathway participates in the pathophysiology of nonalcoholic fatty liver disease.