The relationship between local rates of cerebral glucose utilization (ICMRglc) and glucose transporter expression was examined during physiologic activation of the hypothalamoneurohypophysial system. Three days of water deprivation, which is known to activate the hypothalamoneurohypophysial system, resulted in increased ICMRglc and increased concentrations of GLUT1 and GLUT3 in the neurohypophysis; mRNA levels of GLUT1 and GLUT3 were decreased and increased, respectively. Water deprivation also increased ICMRglc in the hypothalamic supraoptic and paraventricular nuclei; mRNA levels of GLUT1 and GLUT3 appeared to increase in these nuclei, but the changes did not achieve statistical significance. Restoration of water for 3 to 7 days reversed all observed changes in GLUT expression (protein and mRNA): restoration of water also reversed changes in ICMRglc in both the neurohypophysis and the hypothalamic nuclei. These results indicate that under conditions of neural activation and recovery, changes in ICMRglc and the levels of GLUT1 and GLUT3 are temporally correlated in the neurohypophysis and raise the possibility that GLUT1 and GLUT3 transporter expression may be regulated by chronic changes in functional activity. In addition, increases in the expression of GLUT5 mRNA in the neurohypophysis after dehydration provide evidence for involvement of microglial activation.
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http://dx.doi.org/10.1097/00004647-200001000-00024 | DOI Listing |
J Immunother Cancer
January 2025
Biotherapy Center & Cancer Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People's Republic of China
Background: Glucose deprivation inhibits T-cell metabolism and function. Glucose levels are low in the tumor microenvironment of solid tumors and insufficient glucose uptake limits the antitumor response of T cells. Furthermore, glucose restriction can contribute to the failure of chimeric antigen receptor T (CAR-T) cell therapy for solid tumors.
View Article and Find Full Text PDFIntroduction: Advanced glycation end products (AGEs) play a critical role in the development of vascular diseases in diabetes. Although stem cell therapies often involve exposure to AGEs, the impact of this environment on extracellular vesicles (EVs) and endothelial cell metabolism remains unclear.
Methods: Human umbilical cord mesenchymal stem cells (MSCs) were treated with either 0 ng/ml or 100 ng/ml AGEs in a serum-free medium for 48 hours, after which MSC-EVs were isolated.
Sci Adv
January 2025
Translational Research Program in Pediatric Orthopedics, Department of Surgery, The Children's Hospital of Philadelphia, Philadelphia, PA, USA.
The initial interzone cells for synovial joints originate from chondrocytes, but such critical transition is minimally understood. With single-cell RNA sequencing (scRNA-seq) of murine embryonic knee joint primordia, we discovered that heightened expression of glycolysis genes characterized developing interzone cells when compared to flanking chondrocytes. Conditional deletion of the glucose transporters and/or , in either the incipient pre-skeletal mesenchyme with or in chondrocytes with , disrupted interzone formation dose-dependently.
View Article and Find Full Text PDFRedox Rep
December 2025
Department of Clinical Laboratory, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai, People's Republic of China.
Objectives: Bone remodeling imbalance contributes to osteoporosis. Though current medications enhance osteoblast involvement in bone formation, the underlying pathways remain unclear. This study was aimed to explore the pathways involved in bone formation by osteoblasts, we investigate the protective role of glycolysis and N6-methyladenosine methylation (m6A) against oxidative stress-induced impairment of osteogenesis in MC3T3-E1 cells.
View Article and Find Full Text PDFJ Diabetes Investig
December 2024
Department of Reproduction, Poznan University of Medical Sciences, Poznan, Poland.
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