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Effects of leptin and adiponectin on the cardiovascular system Volume 78, issue 3, Mai-Juin 2020

Authors
Jean-Philippe Bastard Pour le groupe de travail RIHN Adipokinesa 2 3 4
1 Laboratoire de biochimie, Institut fédératif de biologie, Hôpital Purpan, CHU de Toulouse, Toulouse, France
2 Sorbonne Université, Inserm UMR_S 938, Centre de recherche Saint-Antoine, Institut hospitalo-universitaire de cardio-métabolisme et nutrition (ICAN), Paris, France
3 Hôpital Tenon, AP-HP, Service de biochimie et hormonologie, UF Bio-marqueurs inflammatoires et métaboliques, Paris, France
4 Hôpitaux universitaires Henri Mondor, AP-HP, Département de biochimie-pharmacologie-biologie moléculaire-génétique médicale, Créteil, France
* Correspondance
a Membres du groupe de travail RIHN Adipokines : Jean-Philippe Bastard, Jacqueline Capeau, Rim Charchour, Christine Collet, Charlotte Cuerq, Diane Dufour-Rainfray, Soraya Fellahi, Annelise Genoux, Jean Guibourdenche, Isabelle Jéru, Jean-Marc Lacorte, Gilles Morineau, Camille Vatier, Corinne Vigouroux

Elevated circulating leptin levels have been associated with an increased cardiovascular risk in humans. However, recent meta-analyses show that certain epidemiological studies did not find this association, suggesting distinct effects of leptin depending on the pathophysiological context. Studies performed in mice deficient in leptin or in leptin receptors are often contradictory, showing both protective and deleterious effects of leptin. These effects appear to vary depending on the genetic background of the animal and the doses of leptin administered, making interpretation of the results difficult. In humans, elevated adiponectinemia is associated with a favourable cardiovascular risk profile. Adiponectin exerts protective effects at all stages of development of atherosclerotic plaque. However, our knowledge of the pathophysiological mechanisms involved in these protective effects has been established from cellular models, which do not necessarily reproduce the pathology in all its complexity. In addition, mouse models have a very different lipoprotein metabolism from humans, which does not always allow extrapolation of results to humans. Finally, epidemiological studies evaluating adiponectin as a marker of cardiovascular risk show paradoxical results since a high serum adiponectin concentration has not been associated with a reduction in the number of cardiovascular events but with an increase of cardiovascular and all causes mortality in healthy subjects and coronary patients. These observations illustrate the paradox of adipokines actions and show the complexity to use these biomarkers in cardiovascular diseases. Resistance to the action of these adipokines is one of the hypotheses put forward to explain these discrepancies.

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