• Obesity and inflammation
  • Leila Asadpour,1 Rouzbeh Sojoudi Masuleh,2,* Homa Khajeh,3
    1. Department Of Microbiology, Rasht Branch,Islamic Azad University, Rasht, Iran
    2. Department of Biological Sciences and Technologies, Islamic Azad University, Rasht Branch, Gilan, Iran
    3. Tehran University of Medical Sciences - School of Allied Medical Sciences


  • Introduction: Since obesity rates have increased rapidly in recent decades, it is now referred to as a global epidemic. The World Health Organization (WHO) estimates that negative health effects from obesity cause at least 2.8 million deaths annually. The prevalence for both metabolic and non-metabolic diseases, including type 2 diabetes (T2D), insulin resistance, hyperglycemia, dyslipidemia, cardiovascular disorders, fatty liver, high blood pressure, and cancer, is higher in obese individuals. Continuous obesity triggers mild inflammations in the body, which can elevate one's susceptibility to a variety of illnesses. Fat position, the state of the immune system, genetics, and even the type of adipose tissue (AT) all possess a significant impact on the inflammation induced by obesity. The passage of immune cells such as neutrophils, eosinophils, and macrophages into inflammatory tissues is one of the key characteristics of inflammation. Based on current studies, as peri-adipocytes, or fat cells, increase, they may begin to release chemotactic signals that attract macrophages. The necrotic fat cells often serve as the immune system's trigger in cases of chronic obesity. Due to their necrosis in obesity-related conditions, these cells stimulate immune system components such as macrophages to produce a cytokine known as tumor necrosis factor-alpha (TNF-α). Long-term obesity can lead to changes in the number of macrophages as well as distinct phenotypes. Under normal circumstances, they can polarize in this manner from the M0 or M2-like phenotype to the inflammatory or M1 phenotype, and they may enhance the inflammation in AT through the release of additional inflammatory cytokines such as TNF-α, IL-1β, and IL-6. Insulin resistance may develop as a result of this cytokine's prolonged secretion, which is one of the factors contributing to type II diabetes (T2D). Investigation has indicated that the generation of inflammatory mediators such as IL-6 and IFN-γ may stimulate mast cells, which in turn induce inflammation in the visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) of obese humans and mice. Obese individual’s SAT and VAT comprise neutrophils, which are likewise active in peripheral blood.
  • Methods: The research's keywords were "inflammation and obesity," "obesity-linked inflammation," and "inflammatory mechanisms in obesity." These terms can be found in well-known obesity-related databases, websites, and journals such as PubMed/Medline, Google Scholar, Elsevier, and Nature. The required information was then extracted and analyzed from these sources of information.
  • Results: Although obesity is prevalent, it is a very treatable and preventable condition. This disease causes mild inflammation, which over time may increase a person's risk of developing conditions like atherosclerosis, type II diabetes, high blood pressure, liver problems, and even cancer. It's fascinating to note that tertiary lymphatic tissues can be induced in obesity-related inflammation by recruiting immune system cells to the site. Obesity may raise the number of ILC1s in SAT, which may then stimulate M1-like macrophages and enhance inflammation in AT through the production of IFN-γ. On the other hand, ILC2s are normally found in the VAT and SAT of humans and mice, decrease with obesity and may be crucial for maintaining eosinophils and M2-like macrophages as well as appropriate AT homeostasis.
  • Conclusion: Despite common belief, the inflammation induced by fat is manageable, even though it can be quite hazardous. It is now widely known that chronic inflammation, especially in AT, has a role in the etiology of T2D and its consequences. Inflammatory pathways are an appealing target for the treatment of metabolic diseases because of the connection between obesity, AT inflammation, and metabolic disease. Obesity may produce inflammation, although its inhibitors may help lessen it. Major inflammatory cytokines such as TNF-α and IL-1β are generated in obesity. Additionally, medications with anti-inflammatory capabilities, such as metformin in different dosages, salsalate, and thiazolidinediones (TZDs), may help lessen inflammation caused by obesity.
  • Keywords: inflammation and obesity, obesity-linked inflammation, inflammatory mechanisms in obesity