Adipokines and the cardiovascular system: mechanisms mediating health and disease

Abstract

This review focuses on the role of adipokines in the maintenance of a healthy cardiovascular system, and the mechanisms by which these factors mediate the development of cardiovascular disease in obesity. Adipocytes are the major cell type comprising the adipose tissue. These cells secrete numerous factors, termed adipokines, into the blood, including adiponectin, leptin, resistin, chemerin, omentin, vaspin, and visfatin. Adipose tissue is a highly vascularised endocrine organ, and different adipose depots have distinct adipokine secretion profiles, which are altered with obesity. The ability of many adipokines to stimulate angiogenesis is crucial for adipose tissue expansion; however, excessive blood vessel growth is deleterious. As well, some adipokines induce inflammation, which promotes cardiovascular disease progression. We discuss how these 7 aforementioned adipokines act upon the various cardiovascular cell types (endothelial progenitor cells, endothelial cells, vascular smooth muscle cells, pericytes, cardiomyocytes, and cardiac fibroblasts), the direct effects of these actions, and their overall impact on the cardiovascular system. These were chosen, as these adipokines are secreted predominantly from adipocytes and have known effects on cardiovascular cells.

The Effects of Wild Blueberry Consumption on Plasma Markers and Gene Expression Related to Glucose Metabolism in the Obese Zucker Rat

“…19 In the liver, resistin increases glucose production and release in the bloodstream, while in peripheral tissues, it interferes with the normal insulin signaling cascade, thus decreasing insulin sensitivity. [19][20][21] In the present study, OZRs had significantly higher plasma circulating levels of resistin and significantly higher resistin expression in the liver compared with LZRs. WB diet significantly reduced plasma resistin in OZRs and downregulated liver resistin expression both in OZRs and LZRs.…”

Metabolic Syndrome Individuals With and Without Type 2 Diabetes Mellitus Present Generalized Vascular Dysfunction

“…Elevated proinflammatory cytokines could explain the depressed vascular dysfunction in macro-and microcirculation beds. This may occur via the known deleterious effect of adipokines on many responses: (1) endothelial NO synthase expression in the endothelial cell resulting in lower NO synthesis and increased endothelin-1, 30 (2) the anticontractile properties of healthy adipose tissue surrounding blood vessels, 31 (3) higher proliferation and contractility of vascular smooth muscle cells, 32 or (4) tetrahydrobiopterin bioavailability resulting in endothelial NO synthase uncoupling, leading to an increase in superoxide anion production and inhibition of endothelial NO synthase/ cGMP signaling. 33 Nonetheless, it must be considered that our study was performed in vivo during normal circulation in humans, and it was not possible to gain more direct insights into release of cytokines.…”

Angiogenesis and Vascular Functions in Modulation of Obesity, Adipose Metabolism, and Insulin Sensitivity

“…For example, whereas leptin induces angiogenesis, vascular fenestration, and vascular remodeling (Bouloumié et al, 1998;Cao et al, 2001;Sierra-Honigmann et al, 1998), adiponectin may inhibit angiogenesis (Brå kenhielm et al, 2004b;Man et al, 2010). Adipose-derived resistin, chemerin, omentin, vaspin, and visfatin are all able to modulate angiogenesis (Bozaoglu et al, 2010;Kim et al, 2007b;Kukla et al, 2011;Mu et al, 2006;Northcott et al, 2012). It appears that some of these proadipokines can synergistically stimulate angiogenesis with known angiogenic factors; examples include leptin plus VEGF and leptin plus FGF-2 (Cao et al, 2001).…”