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( Supplemental Table?1). Fig.?1 shows the distribution of VLDL-C values for PDHS participants with circulating TG values above and below 150?mg/dl, a clinically meaningful cut-point [16]. Notably, there was substantial overlap in VLDL-C in these two groups with non-overlapping TG values suggesting that VLDL-C provides information distinct from total TGs regarding TGRL metabolism. While there was no significant race interaction for VLDL-C association with CAC, there tended to be a gender difference, so results are presented stratified by gender find more as well as for the full sample. VLDL-C levels were positively associated with increasing CAC after adjusting for age, gender, and race, Framingham risk scores, exercise, HbA1c, medication and alcohol use, (Tobit Ratio (TR) 0.38 CI 0.12�C0.65, P?=?0.005) and even after further adjusting for duration of diabetes, BMI, and CRP (TR 0.38 CI 0.12�C0.65, P?=?0.005). Furthermore, addition of plasma apoB levels did not attenuate association of VLDL-C with CAC (TR 0.31 CI 0.03�C0.58, p?=?0.030) ( Table?2). Although the same trends were evident in both genders, there was approximately 3-fold stronger association of VLDL-C with CAC in women than in men (gender interaction P?=?0.034 in Model 1 and P?=?0.048 in Model 4), with statistically significant effects observed in women but not in men ( Table?2). These finding persisted in subgroup analysis in patients not on lipid lowering EPZ5676 ic50 therapy. ( Supplemental Table?2) VLDL-C may relate to CAC and CVD independent of TG levels because cholesterol-rich VLDL particles may impart greater atherogenic risk than total TGs which are distributed across all lipoprotein particles, not just VLDL. Because TG and VLDL-C values were highly correlated, however, their inclusion in models together can lead to excess colinearity and potential spurious findings. Therefore, we compared plasma VLDL-C and TG association with CAC in non-nested models using AIC and BIC scores and found that both AIC and BIC scores were slightly but consistently lower for VLDL-C (e.g., in fully adjusted Model 4; AIC 7263.65, BIC 7402.11) than TG (AIC 7263.94, BIC 7402.40). This suggests that VLDL-C performs better than TG in predicting CAC scores when all other confounders and covariates are held equal. Furthermore, we stratified PDHS participants into MAPK those with TG values below and above 150?mg/dl, a cut-point used in clinical practice. [16] In these stratified analyses, VLDL-C had stronger association with CAC in individuals with TGs >150?mg/dl (TR 0.80, P?=?0.01) than those with TGs