Should Adipokines be Considered in the Choice of the Treatment of Obesity-Related Health Problems?
Vasilios G. Athyros, Konstantinos Tziomalos, Asterios Karagiannis, Panagiotis Anagnostis, Dimitri P. Mikhailidis, Gionata Fiorino, Serena Rovida, Carmen Correale, Alberto Malesci and Silvio Danese
Affiliation: Academic Head, Department of Clinical Biochemistry, Royal Free Hospital Campus, University College Medical School, University College London, Pond Street, London NW3 2QG, UK., Division of Gastroenterology, Istituto Clinico Humanitas-IRCCS in Gastroenterology, Viale Manzoni, Rozzano, Milan, Italy.
Keywords: Obesity-related health problems, adipokines, insulin resistance, diabetes mellitus, cardiovascular disease
White adipose tissue (WAT) is an important endocrine organ that secretes approximately 30 biologically active peptides and proteins, collectively termed “adipokines”. These are either produced exclusively by WAT (mainly adiponectin, leptin and resistin) or also by other tissues [e.g. tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, plasminogen activator inhibitor (PAI)-1, angiotensinogen]. Adipokines play a central role in body homeostasis including the regulation of food intake and energy balance, insulin action, lipid and glucose metabolism, angiogenesis and vascular remodelling, regulation of blood pressure and coagulation. Excess WAT, especially visceral obesity, is linked to obesityrelated health problems through insulin resistance (IR) [leading to type 2 diabetes mellitus (T2DM)] and systemic lowgrade inflammation [leading to cardiovascular disease (CVD)]. The adipokines are important mediators of these adverse effects. This review describes the role of proinflammatory adipokines in the pathogenesis of IR and of the chronic inflammatory state associated with visceral obesity. Moreover, it summarises treatment options for the normalisation of adipokine levels, which might confer an additional clinical benefit in the effort to prevent or treat obesity-related T2DM and CVD.
Rights & PermissionsPrintExport