Adipokines: Deciphering the cardiovascular signature of adipose tissue

Abstract

Obesity and hypertension are intimately linked due to the various ways that the important cell types such as vascular smooth muscle cells (VSMC), endothelial cells (EC), immune cells, and adipocytes, communicate with one another to contribute to these two pathologies. Adipose tissue is a very dynamic organ comprised primarily of adipocytes, which are well known for their role in energy storage. More recently adipose tissue has been recognized as the largest endocrine organ because of its ability to produce a vast number of signaling molecules called adipokines. These signaling molecules stimulate specific types of cells or tissues with many adipokines acting as indicators of adipocyte healthy function, such as adiponectin, omentin, and FGF21, which show anti-inflammatory or cardioprotective effects, acting as regulators of healthy physiological function. Others, like visfatin, chemerin, resistin, and leptin are often altered during pathophysiological circumstances like obesity and lipodystrophy, demonstrating negative cardiovascular outcomes when produced in excess. This review aims to explore the role of adipocytes and their derived products as well as the impacts of these adipokines on blood pressure regulation and cardiovascular homeostasis.

Keywords: Adipocytes; Adipose tissue; Blood pressure; Blood vessels.

Figure1.. Adipocyte’s characterization.

White adipocytes store energy as a single large lipid droplet and have important endocrine functions. Brown adipocytes are smaller than white adipocytes and present multiple lipid droplets and a large number of mitochondria, [rich in Uncoupling Protein 1 (UCP1)], which is associated with thermogenesis. Brown adipocytes present a mild endocrine function. Beige adipocytes or brite adipocytes are an inducible form of thermogenic adipocytes that is found within WAT depots. They present several lipid droplets, but less than brown adipocytes, and a mild endocrine function.

Figure 2.. Pro and anti-hypertensive stimulus caused by adipocytes-derived molecules.

Adipokines can interfere on cardiovascular function by diverse mechanisms: modulating endothelial and vascular function, maintaining the vascular phenotype, acting as an inflammatory regulator via direct mechanisms in the vasculature or immune cells. Furthermore, adipokines can regulate the secretion of other hormones such as aldosterone. Adipokines also regulate the cardiovascular system on a sex dependent manner (leptin induces hypertension in male, dependent on sympathetic activation, whereas in female it depends on aldosterone secretion. NO, nitric oxide; ROS, reactive oxygen species; ET-1, endothelin-1; PPARγ, peroxisome proliferator activated receptor gamma; FGF21, fibroblast growth factor 21; RAAS, renin–angiotensin–aldosterone system; NF-κB, Nuclear factor kappa B; COX2, cyclooxygenase-2.

Figure 3.. Interventions and body fat mass regulation.

In addition to the direct effects on cardiovascular system, physical exercise and balanced diet are known by diminishing the fat content, which is an additional protective mechanism on cardiovascular function. Combination of both is a powerful tool to reduce the cardiovascular risk. Surgical or pharmacological interventions are scientifically proven of reducing the fat mass, but both may have side effects on cardiovascular function including hypertension.

Figure 4.. Maintain the right amount and good quality of adipose tissue are the right thing to do.

High amount of adipose tissue (obesity) is associated with higher risk of cardiovascular disease, similarly, a drastic decrease in adipose tissue (lipodystrophy) increases the cardiovascular disease likely by alternating the levels of adipokines. Thus, keeping a healthy and good quantity of adipose mass can preserve the cardiovascular integrity.