Myosteatosis and Dyslipidemia: Linking Muscle Quality to Cardiometabolic Risk

Myosteatosis, the pathological accumulation of ectopic fat within skeletal muscle, has emerged as a key indicator of impaired muscle quality and metabolic dysfunction. It encompasses intermuscular and intramuscular adipose tissue as well as intramyocellular lipid, which differ in anatomical location, assessment methodology, and metabolic role. This review provides an integrated overview of myosteatosis, focusing on its bidirectional relationship with dyslipidemia. Myosteatosis represents a metabolically active fat depot characterized by heightened lipolytic and pro-inflammatory activity. It serves not only as an energy substrate for muscle contraction but also as a source of lipotoxic intermediates that impair insulin signaling. Dyslipidemia has been proposed to contribute to lipid overflow and ectopic fat deposition in skeletal muscle, whereas myosteatosis-induced insulin resistance may, in turn, be linked to increased hepatic de novo lipogenesis, potentially contributing to atherogenic dyslipidemia. Epidemiological studies consistently demonstrate associations between myosteatosis and adverse lipid profiles across populations, although the magnitude and specificity of these associations vary by sex, age, ethnicity, and accompanying adipose depots such as visceral fat. Most available evidence remains cross-sectional, and standardized quantification methods are lacking. Future longitudinal and interventional studies are needed to clarify causality, define diagnostic thresholds, and determine whether improving muscle quality can mitigate cardiometabolic risk. Incorporating myosteatosis assessment into clinical practice may enhance metabolic risk stratification beyond conventional measures of muscle mass and adiposity.