The variation of lipogenic enzymes and endoplasmic reticulum stress markers expression in high-fat or high-fructose fed mice

Abstract

Objective To explore and compare the mechanism of high-fructose and high-fat diet induced triglyceride excessive accumulation in mice liver and its relationship with endoplasmic reticulum (ER) stress.Methods 45 Adult male C57BL/J6 mice,weight arranged from 25 gram to 30 gram were randomly divided into control group,high-fructose group and high-fat group,15 mice in each group.Common food was fed in control group,high-fructose food was fed in high-fructose group,high-fat food was fed in high-fat group,and the everyday calories consumption in 3 groups was almost equal.Intraperitoneal glucose tolerance test (ipGTT) was performed after feeding for 8 weeks.After mice were sacrificed,triglyceride content,lipogenic enzymes and ER stress markers expression in liver tissues of each group were measured.Results After feeding with different food for 8 weeks,the fat content of epididymis in high-fructose group and high-fat group both was (2.0±0.1) g/100 g (body weight),which was significantly higher than that of control group (1.2 ± 0.1) g/100 g (body weight),P＜0.01).After ipGTT test,the area under curve of blood glucose in high-fructose group and high-fat group was significantly higher than that in control group (P＜0.01).Compared with control group,triglyceride contents of liver tissues in high-fructose group and high-fat group were significantly increased,of those triglyceride contents in high-fructose group increased more obviously,and triglyceride contents in high-fructose group was significantly higher than that of high-fat group (P＜0.01).Compared with control group,the expression of acylCoA carboxylase (ACC),fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD-1) increased in high-fructose group (P＜0.01),while decreased in high-fat group (P＜0.05) ; meanwhile,the expression of phosphorylated pancreatic ER kinase (p-PERK),inositol requiring enzyme 1 (p-IRE-1/t-IRE-1)and glucose-regulated protein 78 (GRP78) was up-regulated in both high-fructose group and high-fat group (all P＜0.01).Conclusion Both high-fructose diet and high-fat diet can induce fatty liver through different mechanisms.High-frucose diet promotes endogenous lipogenesis while high-fat diet inhibits endogenous lipogenesis.Both dietary factors can induce ER stress,which indicate that ER stress is associated with pathogenesis and development of food factors induced fatty liver. Key words: Triglycerides; Fatty liver; Endoplasmic reticulum; Fructose; Diet