Obesity and inflammation: the linking mechanism and the complications

Abstract

Obesity is the accumulation of abnormal or excessive fat that may interfere with the maintenance of an optimal state of health. The excess of macronutrients in the adipose tissues stimulates them to release inflammatory mediators such as tumor necrosis factor α and interleukin 6, and reduces production of adiponectin, predisposing to a pro-inflammatory state and oxidative stress. The increased level of interleukin 6 stimulates the liver to synthesize and secrete C-reactive protein. As a risk factor, inflammation is an imbedded mechanism of developed cardiovascular diseases including coagulation, atherosclerosis, metabolic syndrome, insulin resistance, and diabetes mellitus. It is also associated with development of non-cardiovascular diseases such as psoriasis, depression, cancer, and renal diseases. On the other hand, a reduced level of adiponectin, a significant predictor of cardiovascular mortality, is associated with impaired fasting glucose, leading to type-2 diabetes development, metabolic abnormalities, coronary artery calcification, and stroke. Finally, managing obesity can help reduce the risks of cardiovascular diseases and poor outcome via inhibiting inflammatory mechanisms.

Keywords: C reactive protein; adiponectin; inflammation; interleukin 6; linking mechanism; obesity.

Figure 1

Mechanisms linking abdominal obesity and metabolic syndrome via inflammatory mediators [24] TNF-α – tumor necrosis factor α, IL-6 – interleukin 6, NO – nitric oxide, ROS – reactive oxygen species, JNK – c-jun N-terminal kinase, IKK – inhibitor of k kinase, PKR – protein kinase R.

Figure 2

Effects of adiponectin on insulin sensitivity and peripheral tissues [114]. Adiponectin regulates energy expenditure centrally, decreases lipogenesis and glucose output in the liver, improves the immune system via anti-inflammatory effects, and regulates lipid metabolism genes in adipocytes