Short-term high-fat meal intake alters the expression of circadian clock-, inflammation-, and oxidative stress-related genes in human skeletal muscle

Abstract

Dietary food, depending on timing, amount and composition can influence gene expression in various tissues. Here, we investigated the effect of high-fat meal diets of different compositions on the gene expression pattern of human skeletal muscle. Gene expression data of skeletal muscle samples from human volunteers prior and 4 h after the consumption of high lipid-containing meal consisting of either saturated-, monounsaturated- or polyunsaturated fatty acids were downloaded from the public repository. List of 843 differently expressed genes (DEGs) was generated. Functional analysis revealed that circadian rhythm-, inflammation- and oxidative stress-related genes are highly overrepresented among the DEGs. The magnitude of gene expression changes significantly increases with the saturation level of the dietary fatty acids and the majority of the DEGs are upregulated. We propose that, by altering circadian clock gene expression and inducing inflammation and oxidative stress, high lipid intake can contribute to muscle function decay in the long run.

Keywords:

• Circadian rhythm
• high-fat diet
• inflammation
• oxidative stress
• skeletal muscle

Disclosure statement

Zsolt Sarang was a recipient of Lajos Szodoray fellowship given by the University of Debrecen. The other authors report no conflict of interest.

Data availability

The raw microarray data used in the article can be found deposited in the Gene Expression Omnibus repository (GSE31901). The top 50 up- and downregulated transcripts are included within the supplementary tables.

Additional information

Funding

This work was supported by the National Research, Development and Innovation Office [124244], European Union project titled: Institutional Developments for Intelligent Specialization programme [grant number: EFOP-3.6.1-16-2016-00022 “Debrecen Venture Catapult Program”] and by the GINOP-2.3.2-15-2016-00006 project and EFOP-3.6.3-VEKOP-16-2017-00009 (co-financed by the European Union and the European Regional Development Fund).