Koufakis Theocharis, Kouroupis Dimitrios, Dimakopoulos Georgios, Georgiadis Theofylaktos, Kourti Areti, Doukelis Panagiotis, Zografou Ioanna, Patoulias Dimitrios, Popovic Djordje S, Pyrpasopoulou Athina, Busetto Luca, Kokkinos Alexander, Tsimihodimos Vasilios, Kotsa Kalliopi, Doumas Michael, Makedou Kali
Second Propaedeutic Department of Internal Medicine, Hippokration General Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
BIOSTATS, Epirus Science and Technology Park Campus, University of Ioannina, 45110 Ioannina, Greece.
Biomedicines. 2025 Mar 12;13(3):701. doi: 10.3390/biomedicines13030701.
: Intestinal dysbiosis and systemic inflammation are involved in the pathophysiology of obesity and its complications. Presepsin is a recently discovered inflammation marker, being the soluble form of the bacterial lipopolysaccharide (LPS) receptor. Due to the imbalance of the gut flora and subsequent disruption of the intestinal barrier, circulating LPS levels have been found to be elevated in patients with metabolic diseases, even in the absence of infection. However, to date, no studies have evaluated whether obesity is associated with elevated presepsin levels. : The present study included 81 participants (61.7% women, 27 with obesity, 34 with overweight, and 20 controls with normal body mass index), all free of infection and diabetes mellitus. Presepsin was measured in serum by ELISA, and its concentrations were compared between the groups. : The obesity group had higher presepsin levels compared to controls (8.09 vs. 4.45 ng/mL, = 0.06). When participants with a history of cardiovascular disease were excluded from the analysis and adjusting for multiple confounders through a regression model, the obesity group had higher presepsin values than the overweight and control groups (5.84 vs. 3.32 ng/mL, = 0.016). In contrast, the overweight group had lower concentrations than both the obesity group ( = 0.005) and the controls ( = 0.031). We did not find an association between presepsin and 25-hydroxy vitamin D levels ( = 0.368). : Although the cross-sectional character of the study cannot demonstrate causal relationships, the results could potentially suggest that systemic inflammation is implicated in the pathogenesis of obesity through the disruption of the intestinal barrier. However, the findings should only be seen as hypothesis-generating. The reduction in presepsin in the overweight state is an interesting finding that deserves further investigation.
肠道菌群失调和全身炎症参与肥胖及其并发症的病理生理过程。前降钙素是一种最近发现的炎症标志物，是细菌脂多糖（LPS）受体的可溶性形式。由于肠道菌群失衡及随后肠屏障的破坏，代谢性疾病患者即使在无感染的情况下，循环LPS水平也已被发现升高。然而，迄今为止，尚无研究评估肥胖是否与前降钙素水平升高有关。
本研究纳入了81名参与者（61.7%为女性，27名肥胖者，34名超重者，20名体重指数正常的对照者），所有参与者均无感染和糖尿病。采用酶联免疫吸附测定法（ELISA）检测血清中的前降钙素，并比较各组间的浓度。
与对照组相比，肥胖组的前降钙素水平更高（8.09对4.45 ng/mL，P = 0.06）。当将有心血管疾病病史的参与者排除在分析之外，并通过回归模型对多个混杂因素进行校正后，肥胖组的前降钙素值高于超重组和对照组（5.84对3.32 ng/mL，P = 0.016）。相比之下，超重组的浓度低于肥胖组（P = 0.005）和对照组（P = 0.031）。我们未发现前降钙素与25-羟维生素D水平之间存在关联（P = 0.368）。
尽管该研究的横断面性质无法证明因果关系，但结果可能提示全身炎症通过肠屏障破坏参与肥胖的发病机制。然而，这些发现仅应被视为产生假设。超重状态下前降钙素的降低是一个值得进一步研究的有趣发现。
