12/08/2025
For our Patients the relationship between obesity, body fat and inflammation in autoimmune diseases.
Excess body fat, particularly visceral fat, is a significant source of pro-inflammatory cytokines, which contribute to chronic inflammation and various health issues like insulin resistance and cardiovascular disease. These cytokines, including TNF-α, IL-1β, and IL-6, are released by adipose tissue and can promote inflammation and disrupt normal metabolic processes.
Elaboration:
Fat Tissue as a Source:
Fat tissue, especially abdominal visceral fat, is an active site for the release of pro-inflammatory cytokines.
Pro-inflammatory Cytokines:
These cytokines, such as TNF-α, IL-1β, and IL-6, are involved in regulating various cellular processes, but in excess, they can contribute to inflammation and disease development.
Obesity and Inflammation:
Obesity is linked to increased inflammation due to the release of pro-inflammatory cytokines from excess adipose tissue.
Impact on Insulin Resistance:
The pro-inflammatory cytokines released by fat tissue can impair insulin signaling, leading to insulin resistance, a hallmark of type 2 diabetes.
Cardiovascular Disease:
Chronic inflammation driven by these cytokines is a key factor in the development of cardiovascular diseases, including atherosclerosis and metabolic syndrome.
Other Diseases:
Obesity-related inflammation, mediated by cytokines, is also implicated in the development of various other conditions like psoriasis, depression, cancer, and renal diseases.
Fat Distribution:
While both subcutaneous and visceral fat contribute to inflammation, visceral fat is more metabolically active and releases a greater amount of pro-inflammatory cytokines.
Macrophage Involvement:
In obese individuals, macrophages (immune cells) in adipose tissue can become activated and release pro-inflammatory cytokines, further contributing to the inflammatory state.