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The Effects of Combined Aerobic and Resistance Exercise on Liver Metabolomics in Mice Fed a High-Fat Diet

ABSTRACT:

Background and Objectives: Obesity is often accompanied by hepatic metabolic disorders and chronic low-grade inflammation. While combined aerobic and resistance exercise is considered an intervention to improve body composition, its systematic regulatory effects on the hepatic metabolic profile remain unclear. This study aimed to investigate the effects of 8 weeks of combined aerobic and resistance exercise on the liver metabolomics of high-fat diet-induced obese mice. Methods: Eighteen male C57BL/6J mice were randomly divided into three groups (n = 6 per group): a standard diet control group (C), a high-fat diet model group (HF), and a high-fat diet plus combined exercise group (HFAR). The combined exercise intervention lasted 8 weeks and consisted of treadmill training (12–15 m/min, 30–60 min/day) and ladder climbing with weights (10%–70% of body weight), performed 6 days per week. Liver lipid deposition and pathological changes were assessed using HE and Oil Red O staining; ELISA was used to measure levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and inflammatory factors (IL-1β, IL-6, TNF-α) in the liver; Liquid chromatography–mass spectrometry (LC-MS) non-targeted metabolomics was used to analyze differences in liver metabolites and to perform metabolic pathway analysis. Results: Compared with the HF group, the HFAR group showed significantly lower body weight, fat mass, and body fat percentage (P < 0.01), as well as marked improvements in hepatic steatosis and lipid droplet deposition. Biochemical indicators showed that the combined exercise regimen significantly reduced liver TC, TG, LDL-C, ALT, and AST levels (P < 0.01), increased HDL-C (P < 0.01), and suppressed the overexpression of IL-1β, IL-6, and TNF-α (P < 0.05). Metabolomics analysis identified 20 key differentially expressed metabolites, and metabolic pathway analysis indicated that they were primarily involved in histidine metabolism and fructose/mannose metabolic pathways. Conclusion: Combined aerobic and resistance exercise effectively reduces liver lipid accumulation, inflammation, and damage in high-fat diet-induced obese mice. The mechanism may involve the regulation of histidine metabolism and fructose/mannose metabolic pathways, providing a metabolomic basis for combined exercise interventions in obesity-related liver disease.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS15011 | MetaboLights | 2026-07-11

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS15011_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS15011_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS15011_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_MTBLS15011_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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Project description:Background: Non-alcoholic steatohepatitis (NASH) has become one of the most common liver diseases and is still without approved pharmacotherapy. Lifestyle interventions using exercise and diet change remain the current treatment of choice and even a small weight loss (5-7%) can already have a beneficial effect on NASH. However#the underlying molecular mechanisms of exercise and diet interventions remain largely elusive#and it is unclear whether they exert their health effects via similar or different pathways. Methods: Ldlr-/-.Leiden mice received a high fat diet (HFD) for 30 weeks to establish an advanced state of NASH/fibrosis with simultaneous atherosclerosis development. Groups of mice were then either left untreated (control group) or were treated for 20 weeks with exercise (running wheel)#diet change (switch to a low fat chow diet) or the combination thereof. The liver and distant organs including heart#white adipose tissue (WAT) and muscle were histologically examined. Comprehensive transcriptome analysis of liver#WAT and muscle revealed the organ-specific effects of exercise and diet and defined the underlying pathways. Results: Exercise and dietary change significantly reduced body weight#fat mass#adipocyte size and improved myosteatosis and muscle function with additive effects of combination treatment. WAT inflammation was significantly improved by diet change#tended to be reduced with exercise#and combination therapy had no additive effect. Hepatic steatosis and inflammation were almost fully reversed by exercise and diet change#while hepatic fibrosis tended to be improved with exercise and was significantly improved with diet change. Additive effects for the combination therapy were shown for liver steatosis and associated liver lipids#and atherosclerosis#but not for hepatic inflammation and fibrosis. Pathway analysis revealed complementary effects on metabolic pathways and lipid handling processes#thereby substantiating the added value of combined lifestyle treatment. Conclusions: Exercise#diet change and the combination thereof can reverse established NASH/fibrosis in obese Ldlr-/-.Leiden mice. In addition#the lifestyle interventions had beneficial effects on atherosclerosis#WAT inflammation and muscle function. For steatosis and other parameters related to adiposity or lipid metabolism#exercise and dietary change affected more distinct pathways that acted complementary when the interventions were combined resulting in an additive effect for the combination therapy on important endpoints including NASH and atherosclerosis. For inflammation#exercise and diet change shared several underlying pathways resulting in a net similar effect when the interventions were combined.

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The Effects of Combined Aerobic and Resistance Exercise on Liver Metabolomics in Mice Fed a High-Fat Diet

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