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Updated: Jan 13, 2026
The MPLEx Protocol for Multi-omic Analyses of Soil Samples
Published on: May 30, 2018
Time-course with multi-omics reveals hyperlipidemia dysregulates diurnal rhythms in gut-liver axis
Jinxing Su1, Shangquan Jiang1, Min Chu1
1Center for Stem Cell and Translational Medicine, School of Life Sciences and Medical Engineering, Anhui University, Hefei 230601, Anhui, China; Traditional Chinese Medicine Research Centre, School of Life Sciences and Medical Engineering, Anhui University, Hefei 230601, Anhui, China.
Insights
High-fat diets disrupt the body's internal clock, leading to hyperlipidemia by altering gut microbiota and liver gene expression. This research highlights the gut-liver axis's role in metabolic disease and offers targets for new therapies.
Area of Science:
- * Chronobiology and metabolic disease research.
- * Investigating the interplay between diet, circadian rhythms, and physiological processes.
- * Exploring the gut-liver axis in metabolic health.
Background:
- * Chronic high-fat diet consumption is linked to obesity and hyperlipidemia.
- * Circadian rhythms regulate crucial cardiovascular and metabolic functions.
- * Disruptions in dietary patterns can desynchronize the body's internal clock.
Purpose of the Study:
- * To investigate diurnal rhythm effects on the liver and intestine in a hyperlipidemic mouse model.
- * To identify key genes and microbial taxa involved in circadian metabolic regulation.
- * To elucidate the role of the gut-liver axis in diet-induced metabolic dysregulation.
Main Methods:
- * Transcriptomic, metagenomic, and metabolomic profiling of liver and intestine.
- * Utilized a hyperlipidemic mouse model to study diurnal rhythm effects.
- * Analyzed gene expression, gut microbiota composition, and metabolite profiles.
Main Results:
- * Identified key hepatic circadian clock-regulated genes (e.g., CD36, Hmgcs1) modulating metabolites via the gut-liver axis.
- * Observed diurnal rhythmicity in gut microbiota coordinating intestinal digestion and metabolism.
- * Demonstrated that hyperlipidemia disrupts circadian regulation in the liver and intestine, impacting lipid metabolism.
Conclusions:
- * High-fat diets cause aberrant lipid metabolism gene expression and perturb gut microbiota circadian rhythms.
- * Metabolites act as signaling molecules regulating hepatic lipid metabolism genes via the gut-liver axis.
- * Loss of rhythmic metabolite secretion disrupts circadian gene expression, contributing to hyperlipidemia.
Background:
Chronic overconsumption of high-fat diets contributes to obesity, with hyperlipidemia being a common comorbidity. The cardiovascular system is strongly influenced by diurnal rhythms, which regulate key functions such as endothelial activity, thrombosis, and blood pressure. Diurnal rhythms are central regulators of metabolic and physiological processes, and dietary pattern shifts can disrupt the synchronization of the internal clock within metabolic systems.
Results:
Using a hyperlipidemic mouse model, we investigated diurnal rhythm-related effects on the liver and intestine through transcriptomic, metagenomic, and metabolomic profiling. We identified several key genes-including CD36, Hmgcs1, Ehhadh, Cyp4a12b, Ifi27l2b, Ugt2b1, Ces2a, Cyp3a11, Selenbp2, and Gal3st1-that are regulated by the hepatic circadian clock and modulate metabolites via the gut-liver axis. The gut microbiota exhibited diurnal rhythmicity that coordinates intestinal digestion and metabolism, forming a synergistic circadian metabolic network. Hyperlipidemia disrupted normal circadian regulation in the liver and intestine, affecting lipid synthesis, transport, accumulation, and catabolism.
Discussion:
Our hepatic transcriptomic analysis revealed that a high-fat diet induces aberrant expression of lipid metabolism genes during the night. This diet also perturbs the diurnal rhythm of the gut microbiota, leading to intestinal metabolic dysregulation. Metabolites entering the portal circulation act as signaling molecules that bind to hepatic receptors and directly regulate the transcription of lipid metabolism genes. The loss of rhythmic metabolite secretion consequently disrupts circadian gene expression, contributing to hepatic lipid dysregulation via the gut-liver axis-a key mechanism in hyperlipidemia pathogenesis.
Conclusions:
This study identifies critical temporal windows and core microbial taxa involved in microbiota-metabolite-gene crosstalk via the gut-liver axis, offering a theoretical foundation for diurnal rhythm-targeted interventions in metabolic diseases.
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