Signalling mechanisms underlying the metabolic and other effects of adipokines on the heart

Abstract

Adipokines represent a family of proteins released by adipocytes that affect various biological processes including metabolism, satiety, inflammation, and cardiovascular function. The first adipokine to be identified is leptin, a product of the obesity gene whose primary function is to act as a satiety factor. However, it is now recognized that leptin and many of the newly discovered adipokines produce effects on numerous organ systems including the heart. Indeed, various adipokines including leptin, adiponectin, and apelin exert potent and diverse cardiovascular effects which are mediated by their specific receptors and involve complex and multifaceted cell-signalling pathways. Among these are effects on the heart as well as blood pressure where leptin has been proposed to potentially contribute to obesity-related hypertension. In this review, we focus primarily on the diverse effects of adipokines on the heart and discuss the potential cell-signalling mechanisms underlying their actions. The potential role of adipokines in the regulation of cardiac metabolism and function is discussed. Discussion is also presented on the emerging role, both deleterious and salutary, of various adipokines in heart disease with an examination of the possible underlying mechanisms which contribute to these effects.

Adipokines and cardiovascular disease: A comprehensive review

“…For now, the only conditions where leptin administration has had notable success is in its use in obese patients with mutation of the leptin gene 31 , which led to an almost normalization of weight and also in lipoatrophic diabetes 16 . The literature describes some of the cardioprotective effects of leptin which include reduced extent of myocardial infarction (MI) and protection against reperfusion damage by local autocrine effects (the heart itself also produces leptin) probably mediated through NO and also antilipotoxic effects 32 . Nevertheless, most authors consider leptin one of the 'bad' adipokines in its effect on the cardiovascular (CV) system.…”

Serum leptin concentrations in adolescents and young adults with growth hormone deficiency

“…LEP działa modulująco na wydzielanie horonów przysadkowych, stymulując wydzielanie TRH, GnRH, GH, PRL oraz hamując sekrecję ACTH [12][13][14]. W układzie sercowo-naczyniowym LEP może działać kardioprotekcyjnie, zmniejsza rów-nież toksyczne działanie lipidów zgromadzonych poza tkanką tłuszczową, w tym również w myocardium [15,16].…”

“…Niedobór GH może przyczyniać się do rozwoju zaburzeń w funkcjonowaniu tkanki tłuszczowej, a wiele zaburzeń stwierdzanych u nieleczonych osób z SNP pokrywa się ze spektrum działania leptyny [5][6][7][8][9][10][11][12]15,16,[22][23][24][25][26][27][28][29][30].…”

The differences in the relationship between diastolic dysfunction, selected biomarkers and collagen turn-over in heart failure patients with preserved and reduced ejection fraction

“…Leptin is an adipokine which attenuates the LV hypertrophy and improves diastolic function of the heart [14]. Adiponectin may play an important role in protection against cardiac remodeling by attenuating myocardial hypertrophy [15]. Galectin receptors have been detected in macrophages in dysfunctional hearts and galectin-3 was suggested to correlate with echocardiographic indices of diastolic function [16].…”