Type 1 diabetes (T1D) is a serious chronic autoimmune condition. Even though the root cause of T1D development has yet to be determined, enough is known about the natural history of T1D pathogenesis to allow study of interventions that may delay or even prevent the onset of hyperglycemia and clinical T1D. Primary prevention aims to prevent the onset of beta cell autoimmunity in asymptomatic people at high genetic risk for T1D. Secondary prevention strategies aim to preserve functional beta cells once autoimmunity is present, and tertiary prevention aims to initiate and extend partial remission of beta cell destruction after the clinical onset of T1D. The approval of teplizumab in the United States to delay the onset of clinical T1D marks an impressive milestone in diabetes care. This treatment opens the door to a paradigm shift in T1D care. People with T1D risk need to be identified early by measuring T1D related islet autoantibodies. Identifying people with T1D before they have symptoms will facilitate better understanding of pre-symptomatic T1D progression and T1D prevention strategies that may be effective.
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http://dx.doi.org/10.1016/j.phrs.2023.106792 | DOI Listing |
J Clin Endocrinol Metab
January 2025
Children's Hospital of Philadelphia, Philadelphia, PA, 19104.
Objective: Glycemic outcomes in youth with type 1 diabetes (T1D) in the United States using the two most common automated insulin delivery (AID) systems, Insulet Omnipod 5 (OP5) and Tandem Control IQ (CIQ), have not been compared. We performed the first head-to-head analysis of changes in glycemic metrics among youth initiating AID.
Methods: This single center, retrospective study included youth <21 years with T1D, who started OP5 or CIQ between 1/2020 and 12/2023, and had ≥70% CGM active time.
Extracell Vesicles Circ Nucl Acids
November 2024
The Tenth Affiliated Hospital, Southern Medical University (Dongguan People's Hospital), Dongguan 523059, Guangdong, China.
Recent findings have indicated that the deficiency of inhibitory programmed cell death ligand 1 (PD-L1) and galectin-9 (Gal-9) in pancreatic β-cells is associated with the progression of type 1 diabetes (T1D). This suggests that exogenous PD-L1 and Gal-9 may have promising potential as therapeutics for the treatment of T1D. In light of these reports, a recent work investigated the potential of artificial extracellular vesicles (aEVs) with the presentation of PD-L1 and Gal-9 ligands (PD-L1-Gal-9 aEVs) as a treatment for T1D, with the findings published in .
View Article and Find Full Text PDFConfl Health
January 2025
School of Population Health, RCSI University of Medicine and Health Sciences, Dublin, Ireland.
Background: Humanitarian crises bring unique, and potentially growing challenges to people with type 1 diabetes (T1D). We aimed to determine, in youth with T1D (mean age (± 1SD) 0-17.9 years) within and coming from humanitarian crises settings (HCS), the reported prevalence that meet international consensus targets for glycaemic, blood pressure and lipid management, and incidence of severe hypoglycaemia or diabetic ketoacidosis.
View Article and Find Full Text PDFJ Psychiatr Res
January 2025
Center for Population Health Research, National Institute of Public Health, Cuernavaca, Morelos, Mexico. Electronic address:
Introduction: Whether in utero exposure to pregestational (type 2 [T2D] and type 1 diabetes [T1D]) and gestational diabetes (GDM) are contributing factors in the rise of neurodevelopmental alterations such as autism is yet unclear. Therefore, we summarized the evidence from studies that assessed such association.
Methods: A systematic review with meta-analyses was performed following the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines; eligible studies were identified in PubMed, Web of Science, and EBSCO up to April 3rd, 2023.
Diabetes Obes Metab
January 2025
National Engineering Research Center for Biomaterials, College of Biomedical Engineering, Sichuan University, Chengdu, Sichuan, People's Republic of China.
Aim: To achieve glucose-activated transcriptional regulation of insulin analogue in skeletal muscle of T1D mice, thereby controlling blood glucose levels and preventing or mitigating diabetes-related complications.
Materials And Methods: We developed the GANIT (Glucose-Activated NFAT-regulated INSA-F Transcription) system, an innovative platform building upon the previously established intramuscular plasmid DNA (pDNA) delivery and expression system. In the GANIT system, skeletal muscle cells are genetically engineered to endogenously produce the insulin analogue INSA-F (Insulin Aspart with Furin cleavage sites).
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