Key result
Energy restriction increased Sirt-1 by 63.6 pg/mL (95% CI 1.5-125.7) and atorvastatin reduced LDL-c by 40.0 mg/dL (95% CI -69.9 to -10.1) in women with premature coronary artery disease.
Why the study?
HDL function has shown greater predictive capacity for risk in early coronary artery disease than traditional parameters, but the influence of dietary energy restriction and atorvastatin on HDL function remains unclear.
Does energy restriction or atorvastatin improve biochemical markers, Sirt-1, and HDL function in women with premature coronary artery disease?
RCT (n=39)
randomized
Does energy restriction or atorvastatin improve biochemical markers, Sirt-1, and HDL function in women with premature coronary artery disease?
Mean Difference: 63.6 (95% CI 1.5–125.7)
p-value: p=0.045
In women with premature coronary artery disease, energy restriction increases Sirt-1 and reduces BMI, while atorvastatin reduces LDL-c, with both interventions independently altering HDL function.
Supports adjunctive energy restriction with atorvastatin for biomarker modulation in premature CAD; extends evidence on independent Sirt-1 and HDL effects.
Introduction: HDL function has gained prominence in the literature as there is a greater predictive capacity for risk in early coronary artery disease when compared to the traditional parameters. However, it is unclear how dietary energy restriction and atorvastatin influence HDL function. Methods: A randomized controlled trial with 39 women with early CAD divided into three groups (n = 13): energy restriction (30% of VET), atorvastatin (80 mg), and control. Analyses of traditional biochemical markers (lipid and glucose profile), circulating Sirt-1, and HDL function (lipid composition, lipid transfer, and antioxidant capacity). Results: Participants’ mean age was 50.5 ± 3.8 years. Energy restriction increased Sirt-1 by 63.6 pg/mL (95%CI: 1.5–125.7; p = 0.045) and reduced BMI by 0.8 kg/m2 (95%CI: −1.349–−0.273; p = 0.004) in a manner independent of other cardiometabolic factors. Atorvastatin reduced LDL-c by 40.0 mg/dL (95%CI: −69.910–−10.1; p = 0.010). Increased Sirt-1 and reduced BMI were independently associated with reduced phospholipid composition of HDL (respectively, β = −0.071; CI95%:−0.136–−0.006; p = 0.033; β = 7.486; CI95%:0.350–14.622; p = 0.040). Reduction in BMI was associated with lower HDL-free cholesterol (β = 0.818; CI95%:0.044–1.593; p = 0.039). LDL-c reduction by statins was associated with reduced maximal lipid peroxide production rate of HDL (β = 0.002; CI95%:0.000–0.003; p = 0.022) and total conjugated diene generation (β = 0.001; CI95%:0.000–0.001; p = 0.029). Conclusion: This study showed that energy restriction and atorvastatin administration were associated with changes in lipid profile, serum Sirt-1 concentrations, and HDL function.
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Leal et al. (2022) conducted an RCT in Premature coronary artery disease (n=39). Energy restriction or atorvastatin vs. Control was evaluated on Circulating Sirt-1 (MD 63.6, 95% CI 1.5-125.7, p=0.045). Energy restriction increased Sirt-1 by 63.6 pg/mL (95% CI 1.5-125.7) and atorvastatin reduced LDL-c by 40.0 mg/dL (95% CI -69.9 to -10.1) in women with premature coronary artery disease.
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