Type 2 diabetes (T2D) is a widespread metabolic disorder marked by hyperglycemia, arising from insulin resistance and relative insulin deficiency. This review investigates the critical role of Na+/K+-ATPase (NKA), a transmembrane protein essential for maintaining cellular ion gradients, in the pathophysiology of T2D. We provide an overview of NKA's biological functions, emphasizing its involvement in cellular signaling pathways, insulin secretion, and glucose homeostasis. The potential of NKA as a therapeutic target for T2D is analyzed, showcasing innovative strategies such as NKA activators, gene therapy, and stem cell therapy aimed at enhancing NKA activity to achieve better glycemic control. Additionally, NKA's multifunctional role in maintaining cell viability and modulating immune responses in islet transplantation may offer potential benefits for improving transplant outcomes. By elucidating the complex interactions between NKA and T2D, this review aims to shed light on developing novel therapeutic interventions that meet the multifaceted needs of individuals suffering from this chronic condition, ultimately improving their health outcomes.
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http://dx.doi.org/10.3389/fimmu.2025.1555310 | 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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