Obesity is a disease that occurs as a result of excess adipose tissue, which has many endocrine and metabolic functions in the body, and can lead to physiological, organic, systemic, systemic, hormonal, metabolic, aesthetic, psychological and social problems, and its prevalence has increased greatly in recent years with environmental changes. Inflammation is the body's natural response to injury, infection or harmful stimuli. This includes activation of immune cells, release of cytokines and increased blood flow to the affected area. However, chronic inflammation, unlike acute inflammation, persists over time, potentially leading to tissue damage and can contribute to various chronic diseases.
Inflammation and altered immune response are two important components of obesity. These components play a major role in the development of obesity-related metabolic diseases. The source of chronic systemic inflammation associated with obesity is dysfunction of adipose tissue. Adipose tissue is a special type of connective tissue and is composed of adipocytes. Adipose tissue accounts for 10-15% of body weight in normal weight men and 15-20% in women. In addition to energy storage, storage of fat-soluble vitamins, physical protection and thermogenesis functions of adipose tissue, proteins derived from adipocytes and adipose stromal cells have been shown to have both local and systemic effects of autocrine, paracrine and endocrine origin. When adipose tissue is inflamed, it releases inflammatory mediators that regulate appetite and can affect pathways in the brain. This leads to resistance of leptin, also known as satiety hormone, a metabolic hormone involved in maintaining normal weight. The main function of leptin is to signal to the brain that fat stores are sufficient. In this way, the person realizes that he or she is full and can eat less or stop eating. However, with these changes, the body does not respond appropriately to the satiety hormone and appetite increases.
Cytokines are chemical messengers that regulate gene expression. There is increased cytokine production in obesity. Inflammatory cytokines such as TNF-α and IL-6 are secreted at high levels from adipose tissue in individuals with high body fat. These cytokines stimulate CRP in the liver and cause chronic inflammation. For this reason, obesity is the main cause in patients who are generally investigated for elevated CRP. During the Covid-19 period, it was observed that obese patients were more likely to be hospitalized and therefore more likely to lose their lives. The fact that obesity alone is a risk factor does not fully explain the higher incidence of various chronic diseases in these patients. In obesity alone, there is already a persistent, low-grade chronic inflammation. This may impair the immune response and adversely affect the lung parenchyma and bronchi, which may explain the role of excessive inflammatory reactions.
In addition, the release of inflammatory mediators increases with increasing body mass index (BMI), and this silent inflammation leads to many complications and adverse consequences of obesity. These components play a major role in the development of obesity-related metabolic diseases.
The relationship between inflammation and obesity is bidirectional. Obesity not only triggers inflammation, but inflammation can worsen obesity. Chronic inflammation can promote the progression of obesity, while obesity itself can promote inflammation through various mechanisms. Recognizing this interplay makes it important to address the underlying inflammatory processes rather than limiting obesity to weight management alone. Furthermore, inflammation can disrupt the gut microbiota, which plays a critical role in energy balance and metabolism.
In studies examining the effect of bariatric surgery on obesity-related inflammation, it has been observed that chronic diseases and inflammation regress with postoperative weight loss. Normalization of inflammatory mediators can be achieved in morbidly obese patients with weight loss achieved by reducing calorie intake by reducing stomach volume. It is reported that the bariatric surgery procedure and the amount of weight loss affect inflammatory markers, especially after Roux-en-Y gastric bypass and LSG surgeries, there is a significant decrease in CRP, which has a positive effect on the albumin creatinine ratio in urine. The most effective mechanism is the increase in secretion of GLP-1 and many incretins after bariatric surgery and their regression of inflammation. This is the factor that explains why weight loss is much more effective than weight loss with diets.
Understanding the complex interaction between inflammation and obesity is crucial for public health. Lifestyle interventions, especially targeting chronic inflammation, such as dietary changes, exercise and weight loss, can mitigate the negative effects of inflammation on obesity. An anti-inflammatory diet, rich in antioxidants, omega-3 fatty acids and fiber, has shown promise in studies to reduce inflammation and improve metabolic outcomes.
