Medical School, University of Cyprus, Nicosia, Cyprus.
Second Cardiology Department, "Hippokration" Hospital, Aristotle University of Thessaloniki, Greece.
Cytokine. 2021 Feb;138:155364. doi: 10.1016/j.cyto.2020.155364. Epub 2020 Dec 15.
Omentin-1 and vaspin are novel adipokines, and their association with atherosclerosis is still under investigation. The present study aimed to assess the relationship of those adipokines with preclinical, non-significant carotid atherosclerosis and the impact of statin therapy on their levels, suggesting a link between adiposity and atherosclerosis.
Eighty-four statin-free subjects with non-significant, preclinical carotid atherosclerosis and elevated LDL- cholesterol levels (>130 mg/dl) were recruited to receive atorvastatin (from 10 to 80 mg per day) (atorvastatin group - AG group). Forty-six age- and gender-matched healthy individuals, without any chronic disease served as controls (control group - CG). Clinical parameters, metabolic profile, serum omentin-1, vaspin concentrations and ultrasound measurements of carotid thickening were obtained at the beginning and after 12 months.
At baseline, AG showed lower omentin-1 and vaspin serum levels than CG (p ≤ 0.001). Along the entire study population at baseline, omentin-1 levels were independently related to LDL-cholesterol, while vaspin levels were independently associated with hsCRP and the presence of carotid atherosclerosis (p < 0.05). Within AG, 12-months atorvastatin treatment significantly increased omentin-1 (from 202.79 ± 91.41 ng/ml to 262.56 ± 101 ng/ml, p < 0.001) and vaspin concentrations (from 1.29 ± 0.51 ng/ml to 1.70 ± 0.5 ng/ml, p = 0.002). In standard multiple regression analysis, the presence of carotid atherosclerosis related to baseline vaspin levels (β = -0.232, p < 0.001), while the atorvastatin-induced increase of vaspin was independently associated with hsCRP reduction (β = -0.198, p = 0.045).
Low omentin-1 and vaspin serum levels associated with preclinical, non-significant carotid atherosclerosis. Notably, atorvastatin administration significantly increased both adipokines, but the underlying mechanisms and the clinical impact of those changes requires further investigation.
网膜素-1 和内脂素是新型脂肪因子，它们与动脉粥样硬化的关系仍在研究中。本研究旨在评估这些脂肪因子与临床前期、非显著性颈动脉粥样硬化的关系，并研究他汀类药物治疗对其水平的影响，提示肥胖与动脉粥样硬化之间存在联系。
招募 84 名无他汀类药物治疗、临床前期颈动脉粥样硬化且 LDL-胆固醇水平升高（>130mg/dl）的他汀类药物自由受试者，接受阿托伐他汀（10 至 80mg/天）治疗（阿托伐他汀组 - AG 组）。46 名年龄和性别匹配的无任何慢性疾病的健康个体作为对照组（对照组 - CG）。在基线和 12 个月时获得临床参数、代谢谱、血清网膜素-1、内脂素浓度和颈动脉增厚的超声测量值。
AG 组在基线时的血清网膜素-1 和内脂素水平低于 CG 组（p≤0.001）。在整个研究人群的基线水平上，网膜素-1 水平与 LDL-胆固醇独立相关，而内脂素水平与 hsCRP 和颈动脉粥样硬化的存在独立相关（p<0.05）。在 AG 组中，阿托伐他汀治疗 12 个月后，网膜素-1 （从 202.79±91.41ng/ml 增加到 262.56±101ng/ml，p<0.001）和内脂素浓度（从 1.29±0.51ng/ml 增加到 1.70±0.5ng/ml，p=0.002）均显著增加。在标准多元回归分析中，颈动脉粥样硬化的存在与基线内脂素水平相关（β=-0.232，p<0.001），而阿托伐他汀诱导的内脂素增加与 hsCRP 降低独立相关（β=-0.198，p=0.045）。
低血清网膜素-1 和内脂素水平与临床前期、非显著性颈动脉粥样硬化有关。值得注意的是，阿托伐他汀治疗可显著增加这两种脂肪因子，但这些变化的潜在机制和临床影响需要进一步研究。
