Dadarlat-Pop Alexandra, Pop Dana, Procopciuc Lucia, Sitar-Taut Adela, Zdrenghea Dumitru, Bodizs Gyorgy, Tomoaia Raluca, Gurzau Diana, Fringu Florina, Susca-Hojda Silvana, Buzoianu Anca D
Department of Cardiology, "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Department of Cardiology, Clinical Rehabilitation Hospital, Cluj-Napoca, 400347, Romania.
Int J Gen Med. 2021 May 6;14:1727-1737. doi: 10.2147/IJGM.S301285. eCollection 2021.
Leptin, one of the best-known adipocytes, together with the renin-angiotensin-aldosterone system and galectin-3 are important players in inflammation, arterial hypertension and heart failure pathophysiology. Moreover, uninucleotide A1166C polymorphism is associated with hypertension and poor prognosis in heart failure. The aim of the study was to investigate a possible relationship between leptin serum values, specific heart failure biomarkers and the presence of AT1 receptor A1166C polymorphism in overweight and obese heart failure patients.
The study included 88 consecutive overweight and obese patients admitted for decompensated heart failure. NT-proBNP, MR-proANP, galectin-3 and leptin levels were determined on the arrival day. Genotyping of the A1166C allele - AT1 receptor gene was performed in all patients in order to find variants.
We found a strong positive correlation (r = 0.347, p = 0.001) between leptin serum concentrations and BMI. Leptin levels were not correlated with heart failure biomarkers (NT-proBNP, MR-proANP and galectin-3). All homozygote CC variants were hypertensive, but we registered no significant difference in genetic AC and AA variants distribution between hypertensive and normotensive. Leptin was not significantly modified by the presence of potentially pathogenic A1166C-AT 1 receptor genotypes (AC + CC). But, galectin-3 was found in higher concentrations in patients with heterozygous and homozygous A1166C mutations.
Overweight and obese patients with heart failure display high leptin serum levels. Leptin does not offer incremental prognostic value in heart failure overweight and obese patients. But, galectin-3 was found in higher concentrations in patients with heterozygous and homozygous A1166C mutations, suggesting a worse prognosis probably due to more advanced cardiac fibrosis.
瘦素是最知名的脂肪细胞因子之一，与肾素 - 血管紧张素 - 醛固酮系统及半乳糖凝集素 - 3 一同在炎症、动脉高血压及心力衰竭病理生理学中发挥重要作用。此外，单核苷酸 A1166C 多态性与高血压及心力衰竭的不良预后相关。本研究旨在探讨超重和肥胖心力衰竭患者血清瘦素水平、特定心力衰竭生物标志物与 AT1 受体 A1166C 多态性之间的可能关系。
本研究纳入了 88 例因失代偿性心力衰竭入院的连续超重和肥胖患者。入院当日测定 N 末端 B 型利钠肽原（NT-proBNP）、中段心房利钠肽前体（MR-proANP）、半乳糖凝集素 - 3 和瘦素水平。对所有患者进行 A1166C 等位基因 - AT1 受体基因的基因分型以寻找变异。
我们发现血清瘦素浓度与体重指数（BMI）之间存在强正相关（r = 0.347，p = 0.001）。瘦素水平与心力衰竭生物标志物（NT-proBNP、MR-proANP 和半乳糖凝集素 - 3）无关。所有纯合子 CC 变异患者均患有高血压，但我们未发现高血压和血压正常患者之间遗传 AC 和 AA 变异分布的显著差异。瘦素并未因潜在致病性 A1166C - AT1 受体基因型（AC + CC）的存在而发生显著改变。但是，在杂合子和纯合子 A1166C 突变患者中发现半乳糖凝集素 - 3 浓度较高。
超重和肥胖的心力衰竭患者血清瘦素水平较高。瘦素在超重和肥胖心力衰竭患者中未提供额外的预后价值。但是，在杂合子和纯合子 A1166C 突变患者中发现半乳糖凝集素 - 3 浓度较高，这表明预后可能更差，可能是由于更严重的心脏纤维化。
