Obesity Induced Inflammation – A Complex Condition

Elham Alipoor and Mohammad Javad Hosseinzadeh-Attar*

Obesity Induced Inflammation – A Complex Condition.

The occurrence of overweight and obesity has risen around the world. This rate will increase in the future without appropriate interventions. Obesity is a condition with increased percentage of fat mass. Evidence based studies indicate that excess adiposity is accompanied with a proinflammatory state. This low grade chronic inflammation could initiate and progress the metabolic disorders such as insulin resistance, type 2 diabetes, endothelial dysfunction, atherosclerosis and several types of cancers.

There are outstanding differences between obesity induced inflammation and classic inflammation. Classic inflammation originates from the intense immune system response to an insult, results in Basal Metabolic Rate (BMR) increase and usually diminishes over time. In contrast, obesity induced inflammation is chronic, metabolic, moderate, and is associated with a reduced BMR. Some studies suggested the term “metaflammation” for this inflammatory condition.

The interplay between adipokines and inflammatory response may elucidate the process of diseases. In the obese state, the dysregulation of proinflammatory and anti-inflammatory adipokines could partly explain the inflammatory mechanism of obesity and
its related consequences. Furthermore, adipokines could play a potential role in physiopathology of many inflammatory and autoimmune diseases through their endocrine, paracrine and
autocrine activities.

The point that should be noted is that despite the emphasis on the importance of increasing anti-inflammatory factors and targeting the root causes of inflammation rather than merely inhibiting inflammatory factors, most studies have focused primarily on suppression of well-known inflammatory mediators such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-α (TNF-α). This is a great disappointment that these interventions could not remarkably improve the major inflammation associated disorders including glucose homeostasis.

Obes Res Open J. 2015; 2(3): e12-e14.doi: 10.17140/OROJ-2-e005