Reduction in hepatic non-esterified fatty acid concentration after long-term treatment with atorvastatin lowers hepatic triglyceride synthesis and its secretion in sucrose-fed rats

The effect of high-dose simvastatin on free fatty acid metabolism in patients with type 2 diabetes mellitus

“…Previous studies have reported conflicting results regarding the effect of statins on FFA metabolism. Atorvastatin has been shown to decrease hepatic [26] and plasma [27] FFA in rats. The implications of observations in rodents are uncertain, however, considering known species differences in FFA and triglyceride metabolism [28].…”

Atorvastatin decreases serum levels of advanced glycation endproducts (AGEs) in nonalcoholic steatohepatitis (NASH) patients with dyslipidemia: clinical usefulness of AGEs as a biomarker for the attenuation of NASH

“…The decrease in hepatic triglyceride secretion without an increase in hepatic triglyceride concentration, the reduction of hepatic FFA, and the reduction of cholesteryl ester availability derived from newly synthesized cholesterol that limits the secretion of very low density Results are expressed as means ± SD. P values for qualitative data were calculated using Fisher's exact probability test, and the P values for quantitative data were calculated using the Wilcoxon signed-rank test TNF-a tumor necrosis factor-a, FFA free fatty acid, TBARS thiobarbituric acid reactive substances, P-III-P procollagen type III propeptide, HOMA-IR homeostatic model assessment of insulin resistance, IRI immunoreactive insulin, OGTT oral glucose tolerance test, CT computerized tomography * P \ 0.05 and ** P \ 0.001, compared to the values before treatment [28,29]. Furthermore, it is reported that an animal fed a high-cholesterol diet exhibits hepatic steatosis, inflammation, ballooning, and fibrosis, histological features of NASH [30].…”

Efficacy of atorvastatin for the treatment of nonalcoholic steatohepatitis with dyslipidemia

“…Our study was in accordance with these reports and included multiple end point measurement (liver enzymes, adipocytokines, IR, lipid profile, glucose metabolism, and histologic changes before and after treatment). In experimental models, the decrease in hepatic triglyceride secretion without an increase in hepatic triglyceride concentration, the reduction of hepatic FFA, and the reduction of cholesteryl ester availability derived from newly synthesized cholesterol that limits the secretion of very low-density lipoprotein by statins including atorvastatin have been demonstrated [35,36]. Furthermore, a recent report by Kainuma et al [37] has shown that an animal fed a high-cholesterol diet exhibits hepatic steatosis, inflammation, ballooning, and fibrosis, histologic features of NASH.…”