Background/Objectives: Systemic and tissue inflammation play a crucial role in the pathophysiology of cardiometabolic disorders. Presepsin is a newly discovered marker of acute phase inflammation that is produced by monocytes or macrophages in response to bacterial infection and is a soluble fraction of the lipopolysaccharide (LPS) receptor. LPS is an endotoxin that, through the breakdown of the intestinal barrier, penetrates the systemic circulation and is an important bacterial mediator in the pathogenesis of sepsis and septic shock. Methods: A narrative review of the existing literature. Results: A growing body of evidence demonstrates that intestinal dysbiosis is involved in the pathogenesis of diabetes mellitus (DM) and cardiovascular (CV) disease, leading to increased circulating LPS concentrations in people with cardiometabolic disorders, even in the absence of infection. These data provide the theoretical background for a link between presepsin, DM, and CV pathology. Preliminary studies suggest that presepsin levels are downregulated in patients with well-controlled type 2 DM and correlate with continuous glucose monitoring metrics in infection-free individuals with type 1 DM. However, prospective data on the association between presepsin and the risk of diabetic complications are currently lacking. Presepsin has also been found to be elevated in infection-free individuals with myocardial infarction, heart failure, and myocarditis compared to controls and has been shown to correlate with mortality risk in subjects at high CV risk. Conclusions: The clinical utility of presepsin in the monitoring of patients with cardiometabolic disorders warrants further investigation by future studies.

Background/Objectives: 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. Methods: 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. Results: The obesity group had higher presepsin levels compared to controls (8.09 vs. 4.45 ng/mL, p = 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, p = 0.016). In contrast, the overweight group had lower concentrations than both the obesity group (p = 0.005) and the controls (p = 0.031). We did not find an association between presepsin and 25-hydroxy vitamin D levels (p = 0.368). Conclusions: 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.

Systemic inflammation has been recognized as the cause and consequence of metabolic dysregulation in diabetes mellitus (DM). Presepsin has recently emerged as a promising biomarker for the detection of bacterial infections and sepsis. There is evidence that gut dysbiosis results in the increased circulating concentrations of Gram-negative bacteria lipopolysaccharide, the linkage of presepsin, which in turn promotes insulin resistance and correlates with the risk of diabetic complications. Thus, we hypothesized that presepsin could reflect the magnitude of systemic inflammation and metabolic decompensation in patients with DM even in the absence of infection. In this cross-sectional pilot study, we included 75 infection-free individuals with well-controlled (n = 19) and uncontrolled (n = 23) type 2 diabetes (T2D), well-controlled (n = 10) and uncontrolled (n = 10) type 1 diabetes (T1D), and normoglycemic controls (n = 13). Presepsin levels were compared between the groups and potential associations with demographic, clinical, and laboratory parameters were explored. We observed that the duration of DM was associated with presepsin values (p = 0.008). When the participants were classified into the type of DM groups, the presepsin levels were found to be lower in the patients with T2D compared to those with T1D (p = 0.008). However, significance in that case was driven by the difference between the well-controlled groups. After adjusting for the effects of DM duration, presepsin was significantly lower in the well-controlled T2D group compared to the well-controlled T1D group [1.34 (2.02) vs. 2.22 (4.20) ng/mL, p = 0.01]. Furthermore, we adjusted our findings for various confounders, including age, body mass index, and waist circumference, and found that the difference in the presepsin values between the adequately controlled groups remained significant (p = 0.048). In conclusion, our findings suggest that presepsin could potentially serve as a surrogate marker of inflammation and metabolic control in people with DM.

Background/Objectives: Inflammation is a hallmark of diabetes, with interleukin-6 (IL-6) emerging as a key mediator linking immune activation with metabolic regulation. Although IL-6 has been studied in both type 1 (T1D) and type 2 diabetes (T2D), its relationship with glycemic control across diabetes subtypes remains unexplored. Methods: We conducted a cross-sectional pilot study including 82 participants divided into the following subgroups: healthy controls (n = 14), individuals with T1D [n = 11 with glycated hemoglobin (HbA1c) < 7%; n = 11 with HbA1c ≥ 7%] and T2D (n = 21 with HbA1c < 7%; n = 25 with HbA1c ≥ 7%). Demographic, anthropometric, and laboratory parameters were collected. Group comparisons were performed, adjusted for age and body mass index (BMI) to account for significant demographic differences between groups. Correlations between IL-6, high-sensitivity C-reactive protein (hs-CRP), ferritin, and presepsin were evaluated using Spearman’s rank correlation. Results: IL-6 levels were approximately four-fold higher in T1D individuals with HbA1c ≥ 7% compared with controls [fold-change 4.06 (95% CI: 1.36–12.1), p = 0.013], with optimally managed T1D showing a non-significant trend (p = 0.079). No significant differences were observed in T2D groups. Advancing age demonstrated a borderline association with IL-6 (p = 0.068), whereas BMI was not significantly related. IL-6 correlated positively with hs-CRP (ρ = 0.463, p < 0.001), but not with ferritin or presepsin. Conclusions: IL-6 concentrations were significantly elevated in individuals with suboptimally managed T1D compared with controls, independent of age and BMI, suggesting that poor metabolic control amplifies systemic inflammation in autoimmune diabetes. These findings support IL-6 as a biomarker of inflammatory burden in T1D and provide a rationale for larger, longitudinal studies to determine its clinical utility.

Background/Objectives: The role of intestinal dysbiosis as an important driver of inflammation in metabolic disorders is becoming increasingly evident. Beta-defensin 2 is an antimicrobial peptide that contributes to innate immunity, while recently it has been suggested as a novel biomarker of gut dysbiosis. However, its role in obesity remains unexplored. This study aimed to compare circulating beta-defensin 2 levels between individuals with overweight and obesity and lean controls. An additional objective was to explore potential correlations between beta-defensin 2 and other inflammatory markers in this population. Methods: The study population consisted of 81 participants (61.7% females) divided into obesity (n = 27), overweight (n = 34), and normal body mass index (n = 20) groups. All participants were free of infection and diabetes mellitus. Beta-defensin 2, interleukin-6, presepsin, high-sensitivity C-reactive protein (hs-CRP), and ferritin were evaluated in the study groups. Results: We did not find significant differences in beta-defensin 2 levels between the groups (p = 0.936). In contrast, hs-CRP levels were higher in people with obesity compared to the sum of participants in the overweight and control groups (p = 0.044), after adjusting for the effects of age, sex, smoking, and vitamin D status. Furthermore, a positive correlation was established between beta-defensin 2 and presepsin values (p = 0.012). Conclusions: The results of the present study demonstrate that obesity is characterized by an aggravation of inflammation, as expressed by elevated hs-CRP levels. Although the study design cannot prove causal relationships, our findings also suggest that beta-defensin 2 levels correlate with the magnitude of systemic inflammation in infection-free individuals living with obesity. The value of the combined evaluation of different biomarkers in obesity-related outcomes warrants further investigation by larger studies.

Aim: The aim of this study was to evaluate the specificity, sensitivity and accuracy of the Indicator Plaster Neuropad in detecting established Diabetic Autonomic Neuropathy (DAN). Methods: We studied 180 patients with Diabetes Mellitus (DM, mean age 49.5 ± 16 years, 82 with DM type 1). All patients underwent the following Cardiovascular Reflex Tests (CARTs): R-R variation during deep breathing (Mean Circular Resultant (MCR) and standard deviation (SD)), Valsalva maneuver, R-R variability after a rapid change from lying to standing position and postural hypotension. The presence of DAN was established if ≥2 CARTs were abnormal. According to the result the patients were divided into two groups, one with DAN and one without DAN. Assessment with Neuropad was performed also in all patients. Results: Abnormal perspiration with Neuropad (uncompleted or no change in color) was detected in 94 patients. Established DAN was detected in 85 patients. The sensitivity, specificity and accuracy of Neuropad for the diagnosis of established DAN were 87.1%, 78.9% and 82.8%, respectively and area under the curve was 0.846 and 95% CI (0.787, 0.905). Conclusions: Neuropad has high sensitivity, specificity, and accuracy in detecting established DAN, as defined by ≥2 abnormal CARTs.