Objective: Several circular RNAs are associated with important pathophysiological characteristics of gestational diabetes mellitus (GDM). This study intended to measure the expression of circ-PNPT1 in sera of GDM patients and to expound on its values on pregnancy outcomes.
Methods: Totally 104 GDM patients and 71 healthy controls were recruited. The expression pattern of serum circ-PNPT1 was measured by reverse transcription-quantitative polymerase chain reaction. The diagnostic efficacy of circ-PNPT1 and fasting blood glucose (FBG) on GDM was evaluated by receiver operating characteristic (ROC) analysis. Parameters of glycolipid metabolism were determined using automatic biochemical analyzers. The correlation between circ-PNPT1 and glycolipid metabolism parameters was analyzed using Pearson analysis. GDM patients were divided into a high expression group and a low expression group based on the median value of circ-PNPT1 expression. Curves of adverse neonatal outcomes were drawn by Log Rank analysis.
Results: GDM patients exhibited higher circ-PNPT1 expression than healthy controls. The area under the ROC curve of circ-PNPT1 diagnosing GDM was 0.9184 and the cut-off value was 1.435 (90.38% sensitivity, 85.92% specificity). Serum circ-PNPT1 expression was positively correlated with FBG, total cholesterol, and triglyceride in GDM patients. Neonates born to GDM patients with high circ- PNPT1 expression were prone to adverse outcomes.
Conclusion: Circ-PNPT1 was highly-expressed in the sera of GDM patients. Circ-PNPT1 affected glycolipid metabolism and its expression had certain reference values on adverse pregnancy outcomes.
Background: Cellular senescence is associated with the formation and progression of a range of illnesses, including ageing and metabolic disorders such as diabetes mellitus and pancreatic beta cell dysfunction. Ageing and reduced glucose tolerance are interconnected. Often, Diabetes is becoming more common, which is concerning since it raises the risk of a variety of age-dependent disorders such as cardiovascular disease, cancer, Parkinson's disease, stroke, and Alzheimer's disease.
Objectives: The objectives of this study are to find out the most recent research on how ageing affects the functions of pancreatic beta cells, beta cell mass, beta cell senescence, mitochondrial dysfunction, and hormonal imbalance.
Methods: Various research and review manuscripts are gathered from various records such as Google Scholar, PubMed, Mendeley, Scopus, Science Open, the Directory of Open Access Journals, and the Education Resources Information Centre, using different terms like "Diabetes, cellular senescence, beta cells, ageing, insulin, glucose".
Results: In this review, we research novel targets in order to discover new strategies to treat diabetes. Abnormal glucose homeostasis and type 2 diabetes mellitus in the elderly may aid in the development of novel medicines to delay or prevent diabetes onset, improve quality of life, and, finally, increase life duration.
Conclusion: Aging accelerates beta cell senescence by generating premature cell senescence, which is mostly mediated by high glucose levels. Despite higher plasma glucose levels, hepatic gluconeogenesis accelerates and adipose tissue lipolysis rises, resulting in an increase in free fatty acid levels in the blood and worsening insulin resistance throughout the body.
Helicobacter pylori (H. pylori) is the most thoroughly researched etiological component for stomach inflammation and malignancies. Even though there are conventional recommendations and treatment regimens for eradicating H. pylori, failure rates continue to climb. Antibiotic resistance contributes significantly to misdiagnoses, false positive results, and clinical failures, all of which raise the chance of infection recurrence. This review aims to explore the molecular mechanisms underlying drug resistance in H. pylori and discuss novel approaches for detecting genotypic resistance. Modulation of drug uptake/ efflux, biofilm, and coccoid development. Newer genome sequencing approaches capable of detecting H. pylori genotypic resistance are presented. Prolonged infection in the stomach causes major problems such as gastric cancer. The review discusses how H. pylori causes stomach cancer, recent biomarkers such as miRNAs, molecular pathways in the development of gastric cancer, and diagnostic methods and clinical trials for the disease. Efforts have been made to summarize the recent advancements made toward early diagnosis and novel therapeutic approaches for H. pylori-induced gastric cancer.
Background: Obesity often co-exists with metabolic abnormalities, but the results of studies on the relationship between obesity, metabolic abnormalities and the risk of gout are inconsistent.
Objectives: We aimed to study whether there was a mutual regulation between obesity, metabolic abnormalities and the risk of gout.
Methods: We conducted a cross-sectional study to expound the association between obesity based on different metabolic statuses and the risk of gout. Patients were derived from Nationwide Readmission Database (2018 sample).
Results: A total of 9,668,330 records were recruited for analysis from January to December. The risk of gout in the obesity group, metabolic abnormalities group and obesity combined with metabolic abnormalities group was 1.67 times (OR = 1.67, 95%CI 1.64-1.70), 3.12 times (OR = 3.12, 95%CI 3.09-3.15) and 4.27 times (OR = 4.27, 95%CI 4.22-4.32) higher than that in the normal control group. For different metabolic components, OR value was highest in hypertension group (OR = 2.65, 95%CI 2.60-2.70 and OR = 4.85, 95%CI 4.73-4.97), followed by dyslipidemia group (OR = 2.23, 95%CI 2.16-2.30 and OR = 3.74, 95%CI 3.55-3.95) and in hyperglycemia group (OR = 1.73, 95%CI 1.66-1.80 and OR = 2.94, 95%CI 2.78-3.11). Fewer components of metabolic syndrome were associated with a lower risk of gout in both nonobese and obese patients.
Conclusion: When metabolic abnormalities were present, obesity induced a higher risk of gout. Different components of metabolic abnormalities had different effects on the risk of gout occurrence, and the number of metabolic abnormalities was closely related to the risk of gout occurrence. Follow-up and intervention methods targeting obesity and metabolic abnormalities should be considered for patients with gout.
Background: Several studies have identified CD163 as a potential mediator of diabetes mellitus through an immune-inflammation. Further study is necessary to identify its specific mechanism.
Objectives: In this study, we aimed to investigate CD163 as a potential biomarker associated with immune inflammation in diabetes mellitus through a systematic review and bioinformatics analysis.
Methods: We searched PubMed, Web of Science, the Cochrane Library, and Embase databases with a time limit of September 2, 2022. Furthermore, we conducted a systematic search and review based on PRISMA guidelines. Additionally, diabetic gene expression microarray datasets GSE29221, GSE30528, GSE30529, and GSE20966 were downloaded from the GEO database (http://www.ncbi.nlm.nih.gov/geo) for bioinformatics analysis. The PROSPERO number for this study is CRD420222347160.
Results: Following the inclusion and exclusion criteria, seven articles included 1607 patients, comprising 912 diabetic patients and 695 non-diabetic patients. This systematic review found significantly higher levels of CD163 in diabetic patients compared to non-diabetic patients. People with diabetes had higher levels of CRP expression compared to the control group. Similarly, two of the three papers that used TNF- α as an outcome indicator showed higher expression levels in diabetic patients. Furthermore, IL-6 expression levels were higher in diabetic patients than in the control group. A total of 62 samples were analyzed by bioinformatics (33 case controls and 29 experimental groups), and 85 differential genes were identified containing CD163. According to the immune cell correlation analysis, CD163 was associated with macrophage M2, γδ T lymphocytes, macrophage M1, and other immune cells. Furthermore, to evaluate the diagnostic performance of CD163, we validated it using the GSE20966 dataset. In the validation set, CD163 showed high diagnostic accuracy.
Conclusion: This study suggests CD163 participates in the inflammatory immune response associated with diabetes mellitus and its complications by involving several immune cells. Furthermore, the results suggest CD163 may be a potential biomarker reflecting immune inflammation in diabetic mellitus.
Background: In the last few decades, it has been largely perceived that the factors affecting the immune system and its varying pathways lead to the pathological progression of inflammation and inflammatory conditions. Chronic inflammation also contributes to common diseases, such as diabetes mellitus, ischemic heart disease, cancer, chronic renal inflammatory disease, non-alcoholic fatty hepat-ic disease, autoimmune diseases and neurodegenerative diseases.
Objective: Interestingly, plant sources and secondary metabolites from plants have been increasingly employed in managing acute and chronic inflammatory diseases for centuries. Boswellic acids are pentacyclic triterpenoidal moieties obtained from the oleo gum resin of different Boswellia species.
Methods: Detailed data was collected revealing the anti-inflammatory potential of Boswellic acids through various databases.
Result: These are pharmacologically active agents that possess promising anti-inflammatory, anti-arthritic, antirheumatic, anti-diarrheal, anti-hyperlipidemic, anti-asthmatic, anti-cancer, and anti-microbial effects.
Conclusion: Boswellic acids have been in use since ancient times primarily to treat acute and chronic inflammatory diseases. This review discusses the various mechanisms underlying the inflammatory process and the necessity of such natural products as a medication to treat inflammatory diseases. In addition, a discussion has also been extended to understand the primary targets involved in inflammation. The review further explores the therapeutic potential of boswellic acids in.