| Independent of the association of obesity with dyslipidemia, hypertension,
and increased propensity for diabetes, fatness per se is increasingly
recognized as a cardiovascular offender. That adipose tissue releases
a wide range of adipokines, growth factors, enzymes, and enzyme substrates
linked to vascular injury provides a plausible explanation for the
role of fat in vascular disease: tumor necrosis factor-α, leptin, resistin,
interleukin-1, -6, -8, and -18, serum amyloid A, monocyte chemoattractant
protein 1, macrophage inhibitory factor, aortic carboxypeptidase, HEPARIN-binding
epidermal growth factor-like growth factor, vascular endothelial growth
factor, transforming growth factor β, angiotensinogen, cathepsin S, ESTRADIOL,
cortisol, mineralocorticoid releasing factor, and CALCITONIN peptides
are probable fat-derived prothrombotic, proinflammatory, and proatherosclerotic
agents acting in a paracrine and/or endocrine manner. Other adipocyte
products such as adiponectin, transforming growth factor β, and interleukin-10
exert some antiatherogenic effects. The following is a short overview
of how adipose tissue products affect the vasculature. |
