As a multidimensional metabolic disorder, the disability and death rate of type 2 diabetes mellitus (T2DM) has increased over time. T2DM covers a wide range of pathological manifestations ranging from hyperglycemia to multi-organ failure, and it has the potential to evolve into acute complications, including ketosis and chronic complications such as peripheral neuropathy, retinopathy, and nephropathy. T2DM mainly occurs in microvascular and large vessels and thus it is restricted for the clinician to diagnose and prescribe. However, the pathological mechanism and clinical diagnosis are inadequate. High-throughput metabolomics, characterized by non-invasive diagnostic techniques to identify potential biomarkers and distinct stages of T2DM, has been increasingly recognized as a vigorous tool with latent capacity for clinical translation. The pathological stratification of T2DM can significantly reduce disability and mortality rates. By tracing the metabolome and associated pathways from impaired fasting blood glucose or impaired glucose tolerance to severe organ failure, the chief contributions of large, independent population-based cohorts are summarized herein. These results facilitate understanding the pathophysiology and mechanism and supports research in accurate diagnosis, risk prediction, curative effect, distinct stages, and prognosis judgment of T2DM.
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http://dx.doi.org/10.3389/fendo.2025.1501305 | DOI Listing |
J Clin Endocrinol Metab
March 2025
Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University. 1-1-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
Context: In 2023, we employed Dexcom G6 for real-time continuous glucose monitoring (rt-CGM); it showed high usefulness but unsatisfactory accuracy in type 1 diabetes summer camp (camp) participants.
Objective: To assess the usefulness, recommendation and accuracy of a new rt-CGM system in camp, 2024.
Methods: Sensor glucose (SG) concentrations were measured by Dexcom G7 (G7) from 6 days prior to camp.
PLoS One
March 2025
Public Health Research Center, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates.
Introduction: Family history of cardiovascular disease (CVD) is an independent risk factor for coronary heart disease, and the risk increases with number of family members affected. It offers insights into shared genetic, environmental and lifestyle factors that influence heart disease risk. In this study, we aimed to estimate the association of family history of CVD and its risk factors, as well as the number of affected parents or siblings, with the prevalence of major cardiometabolic risk factors (CRFs) such as hypertension, dysglycemia, dyslipidemia and obesity in a sample of young adults.
View Article and Find Full Text PDFJ Immunol
January 2025
Center for Translational Immunology, Benaroya Research Institute, Seattle, WA, United States.
The CD2-depleting drug alefacept (LFA3-Ig) preserved beta cell function in new-onset type 1 diabetes (T1D) patients. The most promising biomarkers of response were late expansion of exhausted CD8 T cells and rare baseline inflammatory islet-reactive CD4 T cells, neither of which can be used to measure responses to drug in the weeks after treatment. Thus, we investigated whether early changes in T cell immunophenotypes could serve as biomarkers of drug activity.
View Article and Find Full Text PDFJ Immunol
January 2025
Department of Biological Sciences, California State University San Marcos, San Marcos, CA, United States.
Obesity is associated with comorbidities including type 2 diabetes, chronic nonhealing wounds, and psoriasis. Normally, skin homeostasis and repair is regulated through the production of cytokines and growth factors derived from skin-resident cells including epidermal γδ T cells. However, epidermal γδ T cells exhibit reduced proliferation and defective growth factor and cytokine production during obesity and type 2 diabetes.
View Article and Find Full Text PDFJ Immunol
February 2025
Orthopedics Department, Central Hospital of Ezhou, Ezhou, China.
Diabetic nephropathy is a severe chronic complication characterized by cytotoxicity, inflammation, and fibrosis, ultimately leading to renal failure. This study systematically investigated the effects of the PARP1 inhibitor PJ-34 on high glucose-induced cytotoxicity, inflammation, and fibrosis in HK-2 cells, as well as its improvement on neuropathic pain response and transforming growth factor β (TGFβ) expression in a type 1 diabetes mellitus diabetic nephropathy mouse model. Through cellular and animal experiments, we observed that PJ-34 significantly enhanced the proliferative capacity of cells damaged by high glucose, reduced apoptosis, and decreased the release of proinflammatory factors TGFα, interleukin-6, and interleukin-1β.
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