RESUMEN
The association of endotoxemia with metabolic syndrome (MS) and low-grade inflammation in type 1 diabetes (T1D) is little-studied. We investigated the levels of lipopolysaccharide (LPS), lipopolysaccharide-binding protein (LBP), endogenous anti-endotoxin core antibodies (EndoCAb IgG and IgM) and high-sensitivity C-reactive protein (hsCRP) in 74 T1D patients with different MS statuses and 33 control subjects. Within the T1D group, 31 patients had MS. These subjects had higher levels of LPS compared to patients without MS (MS 0.42 (0.35-0.56) or no MS 0.34 (0.3-0.4), p = 0.009). MS was associated with LPS/HDL (OR = 6.5 (2.1; 20.0), p = 0.036) and EndoCAb IgM (OR = 0.32 (0.11; 0.93), p = 0.036) in patients with T1D. LBP (ß = 0.30 (0.09; 0.51), p = 0.005), EndoCAb IgG (ß = 0.29 (0.07; 0.51), p = 0.008) and the LPS/HDL ratio (ß = 0.19 (0.03; 0.41, p = 0.084) were significantly associated with log-transformed hsCRP in T1D. Higher levels of hsCRP and EndoCAb IgG were observed in T1D compared to the control (p = 0.002 and p = 0.091, respectively). In contrast to the situation in the control group, LPS did not correlate with LBP, EndoCAb, leukocytes or HDL in T1D. To conclude, endotoxemia is associated with low-grade inflammation, MS and a distinct response to LPS in T1D.
RESUMEN
(1) Background: Little research is conducted on the link between diabetic kidney disease (DKD) progression and diabetic gastroenteropathy in type 1 diabetes (T1D). (2) Methods. We performed a cross-sectional study with 100 T1D patients; 27 of them had progressive DKD, defined as an estimated glomerular filtration rate (eGFR) decline ≥3 mL/min/year or increased albuminuria stage, over a mean follow-up time of 5.89 ± 1.73 years. A newly developed score with 17 questions on gastrointestinal (GI) symptoms was used. Faecal calprotectin was measured by ELISA. Lower GI endoscopies were performed in 21 patients. (3) Results: The gastrointestinal symptom score demonstrated high reliability (Cronbach's α = 0.78). Patients with progressive DKD had higher GI symptom scores compared to those with stable DKD (p = 0.019). The former group demonstrated more frequent bowel movement disorders (p < 0.01). The scores correlated negatively with eGFR (r = -0.335; p = 0.001), positively with albuminuria (r = 0.245; p = 0.015), Hba1c (r = 0.305; p = 0.002), and diabetes duration (r = 0.251; p = 0.012). Faecal calprotectin levels did not differ between DKD groups significantly. The most commonly reported histopathological findings of enteric mucosa were infiltration with eosinophils, lymphocytes, plasmacytes, the presence of lymphoid follicles, and lymphoid aggregates. Conclusion: The progression of DKD is positively correlated with gastrointestinal symptoms; however, more research is needed to clarify the causal relationships of the gut-kidney axis in T1D.
RESUMEN
The incidence of autoimmunity is increasing, to ensure timely and comprehensive treatment, there must be a diagnostic method or markers that would be available to the general public. Fourier-transform infrared spectroscopy (FTIR) is a relatively inexpensive and accurate method for determining metabolic fingerprint. The metabolism, molecular composition and function of blood cells vary according to individual physiological and pathological conditions. Thus, by obtaining autoimmune disease-specific metabolic fingerprint markers in peripheral blood mononuclear cells (PBMC) and subsequently using machine learning algorithms, it might be possible to create a tool that will allow the diagnosis of autoimmune diseases. In this preliminary study, it was found that the peak shift at 1545 cm-1 could be considered specific for autoimmune disease type 1 diabetes (T1D), while the shifts at 1070 and 1417 cm-1 could be more attributed to the autoimmune condition per se. The prediction of T1D, despite the small number of participants in the study, showed an inverse AUC = 0.33 ± 0.096, n = 15, indicating a stable trend in the prediction of T1D based on FTIR metabolic fingerprint data in the PBMC.
