In vitroeffect of leptin on human cardiac contractility

Abstract

Leptin, a hormone produced by adipose tissue, has been linked to many regulatory pathways. Its role in the complex relationship between obesity and CVDis not yet clear. The aim of the present study was to evaluate whether leptin interferes directly with cardiac function regulation, altering its contractile forcecharacter, and hence contributing to different pathological processes. Muscle samples were obtained from human atrial myocardium. Each trial includedtwo samples from the same patient. They were simultaneously electrically stimulated under sustained perfusion to perform isometric contractions.Onesample 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 beforethe treatment and reported as a percentage. A total of ten successful trials were conducted. Exposure to leptin did not yield a statistically significant variationin 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 thecontrol 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 alterthe contractile character of human atrial tissues, even in supraphysiological dosage. These results suggest that leptin does not play a role in short-termcardiac regulation.