Leptin as a mechanistic link between obesity and systemic lupus erythematous.

Abstract

Systemic lupus erythematosus (SLE) is a chronic, multisystemic, heterogenic and complex autoimmune disease. Similarly, obesity is a chronic condition characterized by excessive adipose tissue and a sustained state of inflammation. Both conditions have shown increasing incidence in recent years, with evidence of closely intertwined pathogenesis. Leptin, a peptide hormone derived from adipokines and produced in white adipose tissue, exhibits functions like those of pro-inflammatory cytokines and plays a key role in regulating the immune system. There is a clear connection linking obesity and SLE. Extensive studies indicate that obese patients have a higher susceptibility to developing immunological diseases, such as SLE, often at younger ages and with an elevated risk of complications. Leptin appears to play a significant role in immune responses and has been implicated as a mediator in the pathogenesis of SLE and obesity. This hormone contributes to chronic inflammation and immune dysfunction. Elevated leptin levels have been identified in patients with SLE and have been associated with increased disease risk, higher disease activity, and a greater likelihood of complications. Similarly, increased leptin levels have been observed in individuals with obesity and metabolic syndrome. This evidence suggests that leptin may serve as a biomarker and a potential therapeutic target for managing SLE, particularly in obese patients.