The pathophysiological consequences of obesity are largely based on
morphofunctional changes in visceral adipose tissue. By disrupting all phases of
adipogenesis, visceral obesity causes adipocyte dysfunction with changes in the
adipokine secretion pattern and the onset of local low-grade chronic inflammation or
meta-inflammation. Anatomical position of visceral adipose tissue allows direct
drainage of proinflammatory and prothrombotic adipocytokines into the portal
bloodstream and liver, which play a key role in the pathogenesis of insulin resistance,
metabolic and cardiovascular disorders, forming a complex cardiometabolic syndrome.
The emergence of insulin resistance followed by atherogenic dyslipidemia results in an
increase in extracellular concentrations of free fatty acids and the expansion of ectopic
fat depots primarily in the liver, pancreas, heart, kidneys, skeletal muscles and bones.
Large insulin-resistant fat cells of ectopic fat depots contribute to the development of
insulin resistance and low-grade systemic inflammation by endocrine, paracrine, and
autocrine secretion of proinflammatory molecules such as: interleukin- (IL) - 6, tumor
necrosis factor-alpha (TNF-α), IL-8, IL-1, and others, causing a complex clinical
disorder which yields a number of interrelated risk factors and long-term
cardiometabolic disease risk increase.
Keywords: Adipose tissue, Cardiometabolic syndrome, Ectopic fat depots,
Insulin resistance, Meta-inflammation, Obesity.
