Dietary alpha- and gamma-tocopherol (1:5 ratio) supplementation attenuates adipose tissue expansion, hepatic steatosis, and expression of inflammatory markers in a high-fat-diet-fed murine model

Abstract

Objectives: The aim of this study was to evaluate the effect of the dietary supplementation of an alpha-and gamma-tocopherol mixture (1:5 ratio) in the adipose tissue expansion, hepatic steatosis, and expression of inflammatory markers induced by consumption of a high-fat diet (HFD) in mice. Methods: Male C57BL/6 J mice were fed for 12 wk and divided into the following: 1) control diet (CD; 10% fat, 20% protein, 70% carbohydrates); 2) CD + TF (CD plus alpha-tocopherol: 0.7 mg/kg/d, gamma-tocopherol: 3.5 mg/kg/d); 3) HFD (60% fat, 20% protein, 20% carbohydrates); and 4) HFD + TF (HFD plus alpha-tocopherol: 0.7 mg/kg/d, gamma-tocopherol: 3.5 mg/kg/d). General parameters, adipocyte size, liver steatosis, adipose and hepatic tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) expression, hepatic nuclear factor kappa B (NF-kappa B), and peroxisome proliferator-activated receptor alpha (PPAR-alpha) levels were evaluated. Results: Tocopherol supplementation in HFD-fed mice showed a significant decrease in the body weight (19%) and adipose tissue weight (52%), adipose tissue/body weight ratio (36%), and serum triacylglycerols (56%); a 42% decrease (P < 0.05) of adipocyte size compared to HFD; attenuation of liver steatosis by decreas-ing (P < 0.05) lipid vesicles presence (90%) and total lipid content (75%); and downregulation of inflammatory markers (TNF-alpha and IL-1 beta), along with an upregulation of hepatic PPAR-alpha expression and its downstream-regulated genes (ACOX and CAT-1), and an inhibition of hepatic NF-kappa B activation. Conclusion: The present study suggests that alpha-and gamma-tocopherol (1:5 ratio) supplementation attenuates the adipocyte enlargement, hepatic steatosis, and metabolic inflammation induced by HFD in association with PPAR-alpha/NF-kappa B modulation. (C) 2021 Elsevier Inc. All rights reserved.