To assess whether obesity and steatosis potentiate expression of inflammatory markers in chronic HCV, serum protein and hepatic messenger RNA (mRNA) levels of c-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) were measured in 171 patients with chronic HCV.
CML accumulation was significantly associated with the grade of hepatic steatosis, the grade of hepatic inflammation, and gene expression levels of inflammatory markers PAI-1, IL-8, and CRP.
Liver expression of key genes related to de novo FA synthesis (LXRα, SREBP1c, ACC1, FAS), FA uptake and transport (PPARγ, CD36, FABP4), FA oxidation (PPARα), and inflammation (IL6, TNFα, CRP, PPARδ) were assessed by RT-qPCR in 127 MO women with normal liver histology (NL, n = 13), simple steatosis (SS, n = 47) and non-alcoholic steatohepatitis (NASH, n = 67).
The subcutaneous fat area was larger, free fatty acid level was higher, C-reactive protein was higher and high molecular weight adiponectin was lower in the FL group than the non-FL group.
SelP, ESR and CRP were significantly higher (P<0.05) and FMD ratios were significantly lower (P<0.05) in patients with nonalcoholic steatohepatitis (NASH) when compared to patients with simple steatosis.
In the chronic hepatitis B patients with steatosis, liver function indicators-alanine aminotransferase (ALT) and AST, levels of inflammatory factors-interleukin-2 (IL-2), IL-6 and CRP and glucolipid metabolism indicators-fasting blood glucose (FBG), 2h postprandial blood glucose (2h PBG), fasting insulin (FINS), triacylglycerol (TG), total cholesterol (TC), and low-density lipoprotein (LDL) were significantly higher than those without steatosis (p<0.05).
Anthropometrics, blood pressure, body composition by dual-energy X-ray absorptiometry (DXA), glycemic and lipid profiles, C-reactive protein (CRP), as well as fatty liver quantification by magnetic resonance imaging (MRI) were assessed.
An uncontrolled clinical trial in 39 hypertriglyceridemic patients with steatosis showed reduction of liver fat by 47% and reductions in liver enzymes and C-reactive protein from the baseline when treated with niacin extended-release for 6 months These hypothesis-generating data indicate a novel repurposed use of niacin for NAFLD.