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Articles

Effects of Phytosterol Supplementation on Serum Levels of Lipid Profiles, Liver Enzymes, Inflammatory Markers, Adiponectin, and Leptin in Patients Affected by Nonalcoholic Fatty Liver Disease: A Double-Blind, Placebo-Controlled, Randomized Clinical Trial

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Pages 651-658 | Received 19 Feb 2018, Accepted 15 Apr 2018, Published online: 16 May 2018
 

ABSTRACT

Objective: Considering the high prevalence of nonalcoholic fatty liver disease and based on the evidence about the role of dietary cholesterol in liver inflammation, and also with regard to the effect of phytosterols on the metabolism of cholesterol, we aimed at exploring the therapeutic potential of phytosterol supplementation against nonalcoholic fatty liver disease.

Method: Thirty-eight patients with nonalcoholic fatty liver disease were randomly divided into two groups: The phytosterol group (n = 19) received a 1.6-g phytosterol supplement daily and the control group (n = 19) received 1.6 g starch daily as placebo for an 8-week period. Blood samples of all patients were taken at baseline (week 0) and at the end of the study (week 8) for measurement of lipid profiles, liver enzymes, inflammatory markers, adiponectin, and leptin.

Results: Phytosterol supplementation significantly improved the levels of low-density lipoprotein cholesterol, aspartate aminotransferase, alanine aminotransferase, and tumor necrosis factor alpha compared to the placebo group. On the other hand, there were no significant differences between the two groups in total cholesterol, triglycerides, high-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, ratios of low-density lipoprotein cholesterol/high-density lipoprotein cholesterol and total cholesterol/high-density lipoprotein cholesterol, gamma-glutamyl transferase, interleukin 6, high-sensitivity C-reactive protein, adiponectin, and leptin.

Conclusions: The present study suggested that daily consumption of 1.6 g phytosterols efficiently lowers low-density lipoprotein cholesterol, aspartate aminotransferase, alanine aminotransferase, and tumor necrosis factor alpha in patients with nonalcoholic fatty liver disease.

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Disclosure

No potential conflicts of interest were disclosed.

Acknowledgments

The source of data used in this article was the MSc thesis of Mohammad Ali Javanmardi, a student at Ahvaz Jundishapur University of Medical Sciences.

The authors acknowledge all patients participating in the study and our best friends who helped us in during the study.

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