Chaban Ryan, Buschmann Katja, Ghazy Ahmed, Poplawski Alicia, Wittmann Nadja, Beiras-Fernandez Andres, Vahl Christian-Friedrich
Department of Cardiothoracic and Vascular Surgery, University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, 55131 Mainz, Germany.
Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center of the Johannes Gutenberg University Mainz, Langenbeckstr. 1, 55131 Mainz, Germany.
J Nutr Sci. 2019 Apr 10;8:e12. doi: 10.1017/jns.2019.6. eCollection 2019.
Leptin, a hormone produced by adipose tissue, has been linked to many regulatory pathways. Its role in the complex relationship between obesity and CVD is not yet clear. The aim of the present study was to evaluate whether leptin interferes directly with cardiac function regulation, altering its contractile force character, and hence contributing to different pathological processes. Muscle samples were obtained from human atrial myocardium. Each trial included two samples from the same patient. They were simultaneously electrically stimulated under sustained perfusion to perform isometric contractions. One sample was treated with a high concentration of human recombinant leptin (1 µg/ml). The other was treated with placebo and served as a control. The exhibited contraction forces (CF) and the contraction duration (CD) after 20 min of treatment were normalised by dividing them by the values before the treatment and reported as a percentage. A total of ten successful trials were conducted. Exposure to leptin did not yield a statistically significant variation in both CF and CF. In the treatment group, CF% measured 108 (95 % CI 91, 125) % and CD% measured 95 (95 % CI 90, 101) % after 20 min. In the control group, CF% measured 105 (90 % CI 84, 126) % and CD% measured 92 (95 % CI 80, 105) % after 20 min. We concluded that leptin does not alter the contractile character of human atrial tissues, even in supraphysiological dosage. These results suggest that leptin does not play a role in short-term cardiac regulation.
瘦素是一种由脂肪组织产生的激素，与许多调节途径有关。其在肥胖与心血管疾病（CVD）复杂关系中的作用尚不清楚。本研究的目的是评估瘦素是否直接干扰心脏功能调节，改变其收缩力特性，进而导致不同的病理过程。肌肉样本取自人类心房心肌。每个试验包括来自同一患者的两个样本。在持续灌注下对它们进行同步电刺激以进行等长收缩。一个样本用高浓度的重组人瘦素（1μg/ml）处理。另一个用安慰剂处理作为对照。处理20分钟后的收缩力（CF）和收缩持续时间（CD）通过除以处理前的值进行标准化，并以百分比形式报告。总共进行了十次成功的试验。暴露于瘦素后，CF和CD均未产生统计学上的显著变化。在治疗组中，处理20分钟后CF%为108（95%CI 91,125）%，CD%为95（95%CI 90,101）%。在对照组中，处理20分钟后CF%为105（90%CI 84,126）%，CD%为92（95%CI 80,105）%。我们得出结论，即使在超生理剂量下，瘦素也不会改变人类心房组织的收缩特性。这些结果表明，瘦素在短期心脏调节中不起作用。
