Immunological mechanisms involved in obesity and their role in metabolic syndrome

• Main Authors: Marta Góralska, Monika Majewska-Szczepanik, Marian Szczepanik
• Format: Article
• Language: English
• Published: Index Copernicus International S.A. 2015-12-01
• Series: Postępy Higieny i Medycyny Doświadczalnej
• Subjects: otyłość; adipokiny; zespół metaboliczny; metazapalenie; Obesity; adipokines
• Online Access: http://phmd.pl/gicid/01.3001.0009.6609

In the past 50 years, the occurrence of human obesity has risen dramatically across the globe. The WHO reported that at least 1.9 billion (1.9 × 109) adults are overweight and 600 million are obese, and the numbers are expected to rise dramatically in the future without intervention. The recent increase in human obesity is caused by increased energy intake and reduced energy expenditure that results in a massive increase in adipose tissue, which is generally harmful to our health. Indeed, the increase in human obesity is strongly associated with an increase in many diseases such as type 2 diabetes (T2D), biliary disease, cardiovascular disease, hepatic steatosis, airway disease, neurodegeneration and certain cancers. The metabolic and immune systems are closely linked and functionally dependent. As a result, excessive nutrient consumption associated with obesity can be recognized as a harmful, stress-inducing biological event by innate pattern recognition receptors (PRRs). This activates inflammatory and stress responses in various metabolic tissues, leading to the chronic low-grade inflammation called metabolic inflammation or “metainflammation”. Adipose tissue is mainly composed of adipocytes, although other cell types contribute to its growth and function, including pre-adipocytes, macrophages, lymphocytes, fibroblasts and vascular cells. Obesity can result in profound changes in the cell composition of fat tissue and can lead to the modulation of individual cell phenotypes. Many factors are involved in development of metainflammation, including hypoxia of adipocytes, oxidative stress, endoplasmic reticulum stress, activation of inflammasomes, adipocyte death, activation of TLR and abnormal gut flora.