Associations remnant cholesterol and insulin resistance with metabolic-associated fatty liver disease

Abstract

Background. Remnant cholesterol (RC), a component of triglyceride-rich lipoproteins, has recently gained attention as an emerging metabolic and cardiovascular risk factor. Insulin resistance (IR) is a central mechanism underlying metabolic-associated fatty liver disease (MAFLD) and plays a key role in lipid metabolism disturbances. Increasing evidence suggests that RC may be closely linked to IR and MAFLD; however, the interrelationship among these conditions remains incompletely understood. Objective. This review aims to summarize and critically evaluate current evidence regarding the associations between remnant cholesterol, insulin resistance, and metabolic-associated fatty liver disease, with an emphasis on potential pathophysiological mechanisms and clinical implications. Methods. A narrative review of the literature was conducted, focusing on epidemiological, clinical, and experimental studies that examined remnant cholesterol, insulin resistance, and MAFLD. Relevant articles were identified through published studies in peer-reviewed journals, with particular attention to recent findings. Results. Accumulating evidence indicates that elevated remnant cholesterol levels are associated with insulin resistance and adverse metabolic profiles. Insulin resistance contributes to altered hepatic lipid handling, promoting the accumulation of triglyceride-rich lipoproteins and remnant particles. Clinical and population-based studies have demonstrated significant associations between remnant cholesterol and MAFLD, while mechanistic studies suggest shared pathways involving hepatic lipid accumulation, inflammation, and metabolic dysregulation. Conclusion. Current evidence supports a close relationship between remnant cholesterol, insulin resistance, and MAFLD. Remnant cholesterol may represent an important metabolic marker linking dyslipidemia to hepatic and systemic insulin resistance. Further well-designed clinical studies are required to clarify causality, define clinical thresholds, and determine whether targeting remnant cholesterol could improve metabolic and hepatic outcomes in patients with MAFLD.

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