Insulin resistance was associated with reduced diastolic function (E/A change -0.11; 95% CI -0.17 to -0.05 per 10-fold HOMA-IR increase) and partly mediated the effects of adiposity depots.
Observational
Effect estimate: Beta -0.11 (95% CI -0.17 to -0.05)
BACKGROUND AND AIMS: The separate cardiovascular effects of type 2 diabetes and adiposity remain to be examined. This study aimed to investigate the role of insulin resistance in the relations of visceral (VAT), abdominal subcutaneous (aSAT) adipose tissue and total body fat (TBF) to cardiovascular remodeling. METHODS AND RESULTS: ) aSAT; -0.09 (-0.16;-0.02) per SD (8%) TBF; -0.11 (-0.17;-0.05) per 10-fold increase in HOMA-IR, whereas VAT and TBF were differently associated with left ventricular (LV) end-diastolic volume: -8.9 (-11.7;-6.1) mL per SD VAT; +5.4 (1.1;9.7) mL per SD TBF. After adding HOMA-IR to the model to evaluate the mediating role of insulin resistance, change in E/A was -0.02 (-0.07;0.04) per SD VAT; -0.03 (-0.08;0.02) per SD aSAT; -0.06 (-0.13;0.01) per SD TBF, and change in LV end-diastolic volume was -7.0 (-9.7;-4.3) mL per SD VAT. In women, adiposity but not HOMA-IR was related to higher aortic arch pulse wave velocity. CONCLUSION: Insulin resistance was associated with reduced diastolic function, separately from VAT and TBF, and partly mediated the associations between adiposity depots and lower diastolic function.
Paiman et al. (Wed,) conducted a observational in Adiposity and insulin resistance. Visceral, abdominal subcutaneous, and total body fat; HOMA-IR was evaluated on Cardiovascular remodeling (diastolic function E/A and left ventricular end-diastolic volume) (Beta -0.11, 95% CI -0.17 to -0.05). Insulin resistance was associated with reduced diastolic function (E/A change -0.11; 95% CI -0.17 to -0.05 per 10-fold HOMA-IR increase) and partly mediated the effects of adiposity depots.