Abstract P187: Associations of Body Composition, Inflammation, and Lipids: The Multi-Ethnic Study of Atherosclerosis

Abstract

Background: Prior evidence has linked inflammation with myopenic obesity (MO), a high cardiometabolic risk body composition phenotype characterized by low muscle and high fat mass. Inflammation may also alter lipid metabolism. This study aimed to examine the association between MO and lipids and whether inflammation is one potential mediator of their complex relationship. Methods: We conducted a cross-sectional analysis of 1,421 Multi-Ethnic Study of Atherosclerosis participants with abdominal computed tomography body composition, lipid, and inflammatory marker measurements. The ratio of total skeletal muscle area to total adipose tissue area (SM/AT) at L3-4 was used to identify MO (lowest sex-stratified tertiles of <0.52 in men and <0.44 in women). Principal component analysis was used to reduce six inflammatory markers by patterns of covariation. Parallel mediation analysis was conducted to examine whether the inflammatory components mediated the relationship between SM/AT and lipids, acknowledging the limitations of cross-sectional data. Results: The sample’s mean age was 64±10 years, 52.4% were female, and 42.1% were Caucasian. Participants with MO (n=474), compared to those without (n=947), had lower high-density lipoprotein cholesterol (HDL-C; 49±13 vs. 54±16, p<0.001), higher remnant cholesterol (RC; 28±13 vs. 24±13, p<0.001), and similar low-density lipoprotein cholesterol (LDL-C; 110±32 vs. 113±30, p=0.073). All inflammatory markers were higher in MO (p≤0.002). Parallel mediation analysis showed significant direct effects between SM/AT and both HDL-C and RC, which were mediated by component 1 but not component 2. There was no significant direct or indirect effect between SM/AT and LDL-C (Table 1). Conclusion: Participants with MO exhibited elevated levels of inflammation and unfavorable lipid profiles. Two inflammatory components were identified, one of which (IL-6, CRP, fibrinogen, and leptin) partially mediated the relationship of SM/AT with HDL-C and RC.