Abstract

We hypothesized that the consumption of chia (Salvia hispanica L.) flour (CF) and chia oil (CO) improves metabolic disorders in the liver of Wistar rats (Rattus norvegicus domestica) fed a high-fat and high-fructose (HFHF) diet. The animals were fed a HFHF diet (n = 30) or AIN93-M standard diet (n = 10) for eight weeks. After this period, the animals fed HFHF were divided into three groups (n = 10): HFHF diet, HFHF plus 14.7% of CF, and HFHF plus 4% of CO. Histological and biochemical analyses, gene expression, protein levels related to inflammation, and oxidative stress were evaluated in the liver. The HFHF diet caused lipogenesis, liver steatosis, oxidative stress, and inflammation in the animals. The CF and CO intake increased the liver total antioxidant capacity and superoxide dismutase, decreased nitric oxide levels and liver steatosis. Furthermore, the CF and CO led to the upregulation of Cpt1a and Adipor2, respectively, whereas CF downregulated Srebf1. CO intake decreased blood glucose, triglycerides, and the animals’ body weight. Chia did not show effects on mitigating liver pro-inflammatory status, which it may indicate occurs later. The addition of chia into an unbalanced diet is a good and relevant strategy to reduce liver metabolic disorders caused by the high consumption of fructose and saturated fat.

Highlights

  • High consumption of fructose and saturated fat is related to an increase of noncommunicable chronic diseases, such as obesity, insulin resistance, metabolic syndrome, type 2 diabetes, and mainly, nonalcoholic fatty liver disease (NAFLD)

  • The aim of this study was to evaluate the effects of chia flour (CF) and chia oil (CO) on oxidative stress, liver steatosis, gene expression related to lipogenesis and fatty acid oxidation, and inflammation in the liver of rats fed high-fat and high-fructose (HFHF)

  • Our study demonstrated that the HFHF diet induced liver inflammation, observed by TLR4, TNF, and p65-NF-B proteins levels, without statistical differences among the groups regarding PPAR-α, IL-10 levels, and inflammatory infiltrates (Figure 5)

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Summary

Introduction

High consumption of fructose and saturated fat is related to an increase of noncommunicable chronic diseases, such as obesity, insulin resistance, metabolic syndrome, type 2 diabetes, and mainly, nonalcoholic fatty liver disease (NAFLD). The synthesis of fatty acids by the excess of glucose and mainly fructose is called de novo lipogenesis, which leads to depletion of adenosine triphosphate in the liver It contributes to cellular stress and increases the risk of developing liver-related complications [4]. The increase of adipose tissue is regulated by insulin, which leads to lipolysis of triglycerides (TG), increasing free fatty acids influx, synthesis and retention of lipid in hepatocytes, and the formation of lipotoxic compounds. These mechanisms can alter the enzymatic antioxidant system and increase lipid peroxidation causing a redox imbalance

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