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. 2015 Dec 31;19(4):289-95.
doi: 10.5717/jenb.2015.15122303.

Effect of high-intensity exercise and high-fat diet on lipid metabolism in the liver of rats

MinHwa Suk  1 , YunA Shin  1
Affiliations

Effect of high-intensity exercise and high-fat diet on lipid metabolism in the liver of rats

MinHwa Suk et al. J Exerc Nutrition Biochem. .

Abstract

Purpose: This study investigated the effects of high-intensity exercise (Ex) and high dietary fat intake on lipid metabolism in the liver of rats.

Methods: Male Sprague-Dawley rats were randomly assigned to one of the four groups (n=10 per group) that were maintained on a normal diet (ND) or high-fat diet (HFD) consisting of 30% fat (w/w), with or without exercise on a treadmill at 30 m/min and 8% grade) for 4 weeks (i.e., ND, ND+Ex, HFD, and HFD+Ex groups).

Results: Body weight (p<.001), total plasma cholesterol (TC) (p<.001), triglyceride (TG) (p<.05), and liver TG levels (p<.05) were increased in the HFD group relative to the ND groups, and serum glucose (p<.05), insulin (p<.05), homeostatic model assessment of insulin resistance (HOMA-IR) (p<.01), and liver TG levels (p<.01) were also higher in the HFD group compared to the ND+Ex group. Plasma free fatty acid was elevated in the HFD+Ex group compared to the HFD group (p<.01). With the exception of acetyl coenzyme A carboxylase, the expression of lipid metabolism-related genes in the liver was altered in the Ex groups compared to the control group (p<.05), with genes involved in lipolysis specifically up regulated in the HFD+Ex group compared to the other groups.

Conclusion: Vigorous exercise may increase glucose utilization and fat oxidation by activating genes in the liver that are associated with lipid metabolism compared to that in animals consuming a HFD without exercise. Therefore, high intensity exercise can be considered to counter the adverse effects of high dietary fat intake.

Keywords: High-fat diet; high-intensity exercise training; lipid metabolism; liver.

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Figures

Fig. 1.
Fig. 1.. Expression of lipid metabolism-related genes in the liver. Data are presented as means±standard deviation (n=10 per group): normal diet (ND); high-fat diet (HFD); exercise (Ex); (A): sterol regulatory element binding protein (SREBP)-1C; (B) acetyl coenzyme A carboxylase (ACC); (C) fatty acid synthase (FAS); (D) carbohydrate regulatory element-binding protein (ChREBP); (E) stearoyl coenzyme A desaturase (SCD)-1; and (F) carnitine palmitoyltransferase (CPT)-1α relative to the expression level of β-actin. The mean of triplicate reactions is shown. *p<0.05, **p<0.01, ***p<0.001
Fig. 2.
Fig. 2.. Protein expression of acetyl coenzyme A carboxylase (ACC) in the liver. Data are presented as means±standard deviation SEM (n=10 per group). The experimental groups were ND, normal diet; ND+Ex, normal diet with high-intensity exercise; HFD, high-fat diet; HFD+Ex, high-fat diet with high-intensity exercise: Acetyl Co-A carboxylase (ACC), *p<0.05
See this image and copyright information in PMC

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