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An Experimental Model of Diet-Induced Metabolic Syndrome in Rabbit: Methodological Considerations, Development, and Assessment
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Untargeted Metabolomic Characteristics of Skeletal Muscle Dysfunction in Rabbits Induced by a High Fat Diet
Huimei Fan1, Yanhong Li1, Jie Wang1
1College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, China.
Animals : an Open Access Journal From MDPI
|July 2, 2021
Summary
A high-fat diet significantly alters skeletal muscle metabolism in rabbits, impacting phospholipids, amino acids, and steroids. These changes disrupt mitochondrial function and glucose metabolism, contributing to metabolic disorders.
Area of Science:
- Metabolomics
- Nutritional Science
- Skeletal Muscle Physiology
Background:
- High-fat diets (HFD) are linked to type 2 diabetes and metabolic syndrome globally.
- Skeletal muscle mitochondrial oxidation and insulin resistance are key features, but mechanisms remain unclear.
Purpose of the Study:
- To investigate how HFD induces metabolic dysfunction in rabbit skeletal muscle.
- To identify key metabolites affected by HFD in skeletal muscle.
Main Methods:
- 16 weaned rabbits were divided into standard normal diet (SND) and HFD groups for 5 weeks.
- Untargeted metabolomic analysis using ultra-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) on skeletal muscle tissue.
- Statistical analysis including Principal Component Analysis (PCA) and Partial Least Squares Discriminant Analysis (PLS-DA).
Main Results:
- HFD significantly altered skeletal muscle levels of phospholipids, long-chain acylcarnitines (LCACs), histidine, carnosine, and tetrahydrocorticosterone.
- Skeletal muscle metabolism was significantly upregulated in the HFD group compared to the SND group.
- Identified biomarkers include phospholipids, LCACs, histidine, carnosine, and tetrahydrocorticosteroids, potentially indicating targets for metabolic diseases.
Conclusions:
- HFD disrupts skeletal muscle metabolism by altering phospholipid, amino acid, carnitine, and steroid pathways.
- Specific metabolites like phospholipids, LCACs, histidine, carnosine, and tetrahydrocorticosteroids impair mitochondrial oxidative capacity and glucose metabolism.
- These findings highlight potential physiological targets for mitigating HFD-induced skeletal muscle metabolic disorders.
