The roles of lipids and inflammation in the association between the triglyceride-glucose index and arterial stiffness: evidence from two large population-based surveys

Abstract

Background: The triglyceride-glucose (TyG) index is a risk marker for arterial stiffness; however, the extent to which the TyG index is associated with arterial stiffness via lipids and inflammation remains unknown. The first aim was to probe the relationship between the TyG index and arterial stiffness in two surveys. The second aim was to clarify whether lipids and inflammation mediate this relationship.

Methods: The sample size of 13,726 U.S. individuals from the National Examination Survey (NHANES) and 3,964 Chinese individuals from the China Health and Retirement Longitudinal Study (CHARLS 2015) were enrolled. Weighted multivariate logistic and linear regression models, as well as restricted cubic spline (RCS) and mediation analyses, were utilized to estimate complex relationships between the TyG index, arterial stiffness, lipids (non-high-density lipoprotein cholesterol [non-HDL-C]) and inflammation (C-reactive protein [CRP]) biomarkers.

Results: A total of 3,420 U.S. patients and 992 Chinese patients were diagnosed with increased arterial stiffness. Regression analyses demonstrated that higher quartiles of the TyG index were associated with a greater incidence of increased arterial stiffness (NHANES: OR = 2.610, 95% CI = 2.043-3.334, P < 0.001; CHARLS: OR = 1.579, 95% CI = 1.057-2.360, P < 0.001). Participants with a higher TyG index/higher CRP level or with a higher TyG index/higher non-HDL-C level had the highest incidence of increased arterial stiffness in the two surveys. The results were still consistent when the sensitivity analysis was implemented with stricter clinical cut-off values of non-HDL-C. Mediation analysis verified that lipids (mediated effect: β = 0.012, P < 0.001 in NHANES; β = 0.020, P < 0.001 in CHARLS) and inflammation (mediated effect: β = 0.003, P < 0.001 in NHANES; β = 0.006, P < 0.001 in CHARLS) partially mediated this relationship.

Conclusions: These results indicated a positive linear correlation between the TyG index, non-HDL-C level, CRP level and increased arterial stiffness in two surveys. Furthermore, lipids and inflammation could partly mediate the correlation of the TyG index with arterial stiffness in both surveys.

Keywords: Arterial stiffness; Inflammation; Lipid; Mediation analyses; Triglyceride-glucose (TyG) index.

Fig. 1

The restricted cubic spline curves of TyG index, non-HDL and CRP in the incidence of increased arterial stiffness. The RCS curves of TyG index (A), non-HDL (B) and CRP (C) in the incidence of increased arterial stiffness in NAHNES and the RCS curves of TyG index (D), non-HDL (E) and CRP (F) in the incidence of increased arterial stiffness in CHARLS. Adjusted for age, sex, BMI, UA, HbA1c, smoking, alcohol consumption, diabetes, hypertension, antihypertensive treatment, antidiabetic treatment

Fig. 2

Subgroup analyses for the association of TyG index with increased arterial stiffness in NHANES (A) and CHARLS (B). Adjusted for age, sex, BMI, UA, HbA1c, smoking, alcohol consumption, diabetes, hypertension, antihypertensive treatment, antidiabetic treatment

Fig. 3

Association of discordance/concordance of TyG index, CRP and non-HDL-C (mean value) with increased arterial stiffness in NHANES (A–B) and in CHARLS (C–D). Adjusted for age, sex, BMI, UA, HbA1c, smoking, alcohol consumption, diabetes, hypertension, antihypertensive treatment, antidiabetic treatment

Fig. 4

Association of discordance/concordance of TyG index, CRP and non-HDL-C (3.4mmol/L/4.9mmol/L-cutoffs) with increased arterial stiffness in NHANES(A–B) and in CHARLS (C–D). Adjusted for age, sex, BMI, UA, HbA1c, smoking, alcohol consumption, diabetes, hypertension, antihypertensive treatment, antidiabetic treatment

Fig. 5

Mediation analysis of the relationship between TyG index and increased arterial stiffness. The graphs in (A–C) represented the mediating role of non-HDL and CRP in NHANES (unadjusted); The graphs in (D–F) represented the mediating role of non-HDL and CRP in CHARLS (unadjusted)