Background: The effects of capsaicin on obesity and glucose homeostasis are still controversial and the mechanisms underlying these effects remain largely unknown. This study aimed to investigate the potential relationship between the regulation of obesity and glucose homeostasis by dietary capsaicin and the alterations of gut microbiota in obese diabetic ob/ob mice.Methods: The ob/ob mice were subjected to a normal, low-capsaicin (0.01%), or high-capsaicin (0.02%) diet for 6 weeks, respectively. Obesity phenotypes, glucose homeostasis, the gut microbiota structure and composition, short-chain fatty acids, gastrointestinal hormones, and pro-inflammatory cytokines were measured.Results: Both the low- and high-capsaicin diets failed to prevent the increase in body weight, adiposity index, and Lee's obesity index. However, dietary capsaicin at both the low and high doses significantly inhibited the increase of fasting blood glucose and insulin levels. These inhibitory effects were comparable between the two groups. Similarly, dietary capsaicin resulted in remarkable improvement in glucose and insulin tolerance. In addition, neither the low- nor high-capsaicin diet could alter the α-diversity and β-diversity of the gut microbiota. Taxonomy-based analysis showed that both the low- and high-capsaicin diets, acting in similar ways, significantly increased the Firmicutes/Bacteroidetes ratio at the phylum level as well as increased the Roseburia abundance and decreased the Bacteroides and Parabacteroides abundances at the genus level. Spearman's correlation analysis revealed that the Roseburia abundance was negatively while the Bacteroides and Parabacteroides abundances were positively correlated to the fasting blood glucose level and area under the curve by the oral glucose tolerance test. Finally, the low- and high-capsaicin diets significantly increased the fecal butyrate and plasma total GLP-1 levels, but decreased plasma total ghrelin, TNF-α, IL-1β, and IL-6 levels as compared with the normal diet.Conclusions: The beneficial effects of dietary capsaicin on glucose homeostasis are likely associated with the alterations of specific bacteria at the genus level. These alterations in bacteria induced by dietary capsaicin contribute to improved glucose homeostasis through increasing short-chain fatty acids, regulating gastrointestinal hormones and inhibiting pro-inflammatory cytokines. However, our results should be interpreted cautiously due to the lower caloric intake at the initial stage after capsaicin diet administration.
Coronary plaque rupture is the most common cause of acute coronary syndrome. However, the timely biomarker-based diagnosis of plaque rupture remains a major unmet clinical challenge. Balloon dilatation and stent implantation during percutaneous coronary intervention (PCI) could cause plaque injury and rupture. Here we aimed to assess the possibility of circulating microRNAs (miRNAs) as biomarkers of acute coronary plaque rupture by virtue of the natural model of PCI-induced plaque rupture. Stable coronary artery disease patients underwent PCI with single stent implantation were recruited and a three-phase approach was conducted in the present study: (i) profiling of plasma miRNAs in a group of patients before (0 h) and after balloon dilatation for 1 h (1 h vs. 0 h), (ii) replication of significant miRNAs in the second group of patients (1 h vs. 0 h), (iii) validation of a multi-miRNAs panel in the third group of patients (0.5 h, 1 h vs. 0 h). Out of 24 miRNAs selected for replication, 6 miRNAs remained significantly associated with plaque rupture. In the validation phase, combinations of miR-483-5p and miR-451a showed the highest area under the receiver-operating-characteristic curve (AUC) (0.982; CI: 0.907-0.999) in patients with plaque rupture for 0.5 h; combinations of miR-483-5p and miR-155-5p showed the highest AUC (0.898; CI: 0.790-0.962) after plaque rupture for 1 h. In conclusion, using a profiling-replication-validation model, we identified 3 miRNAs including miR-155-5p, miR-483-5p and miR-451a, which may be biomarkers for the early identification of plaque rupture.
Background/Aims Evidence has shown that several microRNAs (miRNAs) may be involved in coronary plaque rupture and local thrombus. However, the diagnostic ability of these miRNAs in acute myocardial infarction (AMI) is less known. The aim of this study is to explore the diagnostic value of these circulating miRNAs in patients presenting with acute chest pain in the emergency department. Methods and results In a nested case–control study, 140 of 1,206 patients finally diagnosed with AMI were matched with 70 unstable angina and 70 noncardiac chest pain patients. Five candidate miRNAs (miR‐483‐5p, miR‐155‐5p, miR‐451, miR‐19b, and miR‐223) were selected for validation. Among them, miR‐19b, miR‐223, and miR‐483‐5p were significantly higher in AMI patients compared with those without AMI. A multivariate analysis showed that these miRNAs were independent predictors of AMI. The overall areas under the receiver operating curves (AUCs) for miR‐19b, miR‐223, and miR‐483‐5p were 0.74, 0.65, and 0.70, respectively. However, serial sampling in AMI patients showed that these miRNAs already peaked on admission, which was earlier than troponin I. Among 170 patients with a negative troponin result at presentation, a panel of three miRNAs improved the discrimination ability to a clinical model. In 119 patients presenting within 3 hr after chest‐pain onset, the diagnostic accuracy of each miRNAs was higher than Point of care (POC) troponin assay. And a panel of these miRNAs had an AUC of 0.92. Conclusion Circulating miR‐19b, miR‐223, and miR‐483‐5p may provide clinically useful information for diagnosis in the early phases of AMI.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.