Search

INTRODUCTION: Despite known risk factors for developing type 2 diabetes mellitus (T2D), the research community still tries to discover new markers that would widen our diagnostic and therapeutic approach to diabetes. Therefore, research on microRNA (miR) in diabetes thrives. This study aimed to assess the utility of miR-126, miR-146a, and miR-375 as novel diagnostic markers for T2D. METHODS: We examined relative quantities of miR-126, miR-146a, and miR-375 in the serum of patients with established type 2 diabetes mellitus (n = 68) and compared these with a control group (n = 29). We also undertook a ROC analysis of significantly changed miR to examine their use as a diagnostic test. RESULTS: MiR-126 (p < 0.0001) and miR-146a (p = 0.0005) showed a statistically significant reduction in patients with type 2 diabetes mellitus. MiR-126 also proved to be an exceptional diagnostic test in our study cohort, with high sensitivity (91 %) and specificity (97 %). We did not find any difference in our study groups' relative quantities of miR-375. CONCLUSION: The study proved a statistically significant reduction of miR-126 and miR-146a in patients with T2D [ABSTRACT FROM AUTHOR]

Events associated with the progression of Parkinson's disease (PD) are closely related to biomembrane dysfunction. The specific role of membrane composition in the conformational stability of alpha synuclein (αS) has already been well documented. Administration of rotenone is one of the best strategies to initiate PD phenotype in animal models. In the present study, daily exposure (14 weeks) of orally administered rotenone (10 mg/kg) was employed in a mouse model. The mitochondrial complex I inhibition resulted in elevated level of αS in whole tissue homogenate of mouse jejunum. In addition, we identified a strong intra-individual correlation between αS level and the specific esterified fatty acids. The observed correlation depends mainly on the acyl chain length. Based on the obtained results, it is suggested that there is a high potential to manipulate fatty acid homeostasis in modulating αS based pathogenesis of PD, at least in experimental conditions. [ABSTRACT FROM AUTHOR]

Targeting metabolomic pathways is a promising strategy for cancer treatment. Alterations in the metabolomic state have also an epigenetic impact, making the metabolomic studies even more interesting. We explored metabolomic changes in the blood plasma of patients with primary and secondary lung cancer and tried to explore their origin. We also applied a discrimination algorithm to the data. In the study, blood samples from 132 patients with primary lung cancer, 47 with secondary lung cancer, and 77 subjectively healthy subjects without any cancer history were used. The samples were measured by NMR spectroscopy. PCA and PLS-DA analyses did not distinguish between patients with primary and secondary lung tumors. Accordingly, no significantly changed levels of plasmatic metabolites were found between these groups. When comparing with healthy controls, significantly increased glucose, citrate, acetate, 3-hydroxybutyrate, and creatinine balanced with decreased pyruvate, lactate, alanine, tyrosine, and tryptophan were found as a common feature of both groups. Metabolomic analysis of blood plasma showed considerable proximity of patients with primary and secondary lung cancer. The changes observed can be partially explained as cancer-derived and also as changes showing ischemic nature. Random Forrest discrimination based on the relative concentration of metabolites in blood plasma performed very promising with AUC of 0.95 against controls; however noticeable parts of differencing metabolites are overlapping with those observed after ischemic injury in other studies. [ABSTRACT FROM AUTHOR]