Abstract
Obesity is associated with altered gut microbiota and low-grade inflammation. A key factor in the inflammatory process is endotoxin lipopolysaccharide (LPS). Plasma LPS levels and sensory agent lipopolysaccharide-binding protein (LBP) are shown to be elevated in obesity. This elevation may be due to increased intestinal permeability and incorporation of a high-fat diet accompanied by overfeeding. Bariatric surgery has become a popular treatment option that results in stable weight loss and improvement of obesity-related conditions. Studies outlined in this review show reduced LPS and LBP levels after different bariatric procedures. LPS receptor CD14 and mRNA expression toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4) were also shown to have reduced levels following surgery. Changes in LPS and LPS components after bariatric surgery are shown to be linked to the surgical technique of the procedure and restriction of caloric intake. Additionally, changes in the gut microbiota provide some insight to the reduction of inflammatory markers after surgery. The beneficial effects of bariatric surgery are not dependent on weight loss alone. The inflammatory pathway plays a key role in the improvement of metabolic complications following surgery that should be further examined. Additional research is needed to evaluate short- and long-term changes of LPS and LPS components after bariatric surgery, including how those assessments can be applied to clinical practice.
