The Effects of Sleeve Gastrectomy on Fractalkine

Morbid obesity is an immunometabolic disorder characterized by chronic low-grade inflammation and is associated with type 2 diabetes, cardiovascular diseases, and several malignancies. The inflammatory process accompanying obesity originates primarily within the adipose tissue and gradually evolves into a systemic response, affecting multiple organ systems. Adipocyte hypertrophy and immune-cell infiltration promote the production of proinflammatory mediators, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP). This persistent inflammatory state, commonly referred to as "metaflammation," plays a central role in the development of metabolic dysfunction. Consequently, obesity is currently regarded not merely as a disorder of energy imbalance but as a complex systemic disease in which chronic inflammation contributes substantially to multisystem involvement.

In recent years, laparoscopic sleeve gastrectomy (LSG) has become one of the most frequently performed bariatric procedures worldwide. In addition to achieving substantial and sustained weight loss, LSG is associated with improvements in insulin sensitivity, glycemic control, and lipid metabolism. A considerable proportion of these beneficial effects is believed to be mediated by alterations in inflammatory pathways. However, the dynamics of the postoperative immunometabolic response and its reflection on circulating biomarkers remain incompletely understood.

Fractalkine (CX3CL1) is a unique chemokine that exists in both membrane-bound and soluble forms and regulates leukocyte adhesion and chemotaxis through its receptor CX3CR1. Growing evidence suggests that the CX3CL1/CX3CR1 signaling axis contributes to obesity-associated adipose tissue inflammation and insulin resistance. Increased circulating and adipose tissue levels of CX3CL1 have been reported in obese individuals, and this molecule has been implicated in enhancing monocyte-adipocyte interactions. Nevertheless, the precise role of fractalkine in metabolic regulation remains unclear, and conflicting findings have been reported.

The rapid weight loss and remodeling of inflammatory responses observed after bariatric surgery may also influence the circulating fractalkine levels. However, published data evaluating temporal changes in serum fractalkine levels following laparoscopic sleeve gastrectomy and their relationship with weight loss outcomes remain limited. This knowledge gap raises the possibility that fractalkine may reflect not only weight loss but also the underlying immunometabolic processes associated with obesity and its surgical treatment.

Therefore, the aim of the present study was to evaluate the temporal changes in serum CX3CL1 levels in morbidly obese patients undergoing laparoscopic sleeve gastrectomy and to investigate the relationship between these changes and postoperative weight loss. We also sought to determine whether metabolic alterations after bariatric surgery were associated with changes in circulating CX3CL1 levels.

Inclusion criteria

• • Age ≥18 years
• • Elective laparoscopic sleeve gastrectomy
• • Provision of written informed consent for study participation and scheduled follow-up assessments

Exclusion criteria

• • Active infection or acute inflammatory condition
• • Autoimmune or chronic inflammatory disease
• • History of malignancy
• • Chronic liver or kidney disease
• • Pregnancy or lactation
• • Corticosteroid or immunosuppressive therapy
• • Major postoperative complications
• • Missing data or incomplete sampling