ATP-dependent sugar transport complexity in human erythrocytes.

Am J Physiol Cell Physiol

Dept. of Biochemistry and Molecular Pharmacology, Univ. of Massachusetts Medical School, 364 Plantation St., Worcester, MA 01605, USA.

Published: February 2007

Human erythrocyte glucose sugar transport was examined in resealed red cell ghosts under equilibrium exchange conditions ([sugar](intracellular) = [sugar](extracellular), where brackets indicate concentration). Exchange 3-O-methylglucose (3MG) import and export are monophasic in the absence of cytoplasmic ATP but are biphasic when ATP is present. Biphasic exchange is observed as the rapid filling of a large compartment (66% cell volume) followed by the slow filling of the remaining cytoplasmic space. Biphasic exchange at 20 mM 3MG eliminates the possibility that the rapid exchange phase represents ATP-dependent 3MG binding to the glucose transport protein (GLUT1; cellular [GLUT1] of

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127882PMC
http://dx.doi.org/10.1152/ajpcell.00335.2006DOI Listing

Publication Analysis

Top Keywords

sugar transport
8
atp biphasic
8
biphasic exchange
8
exchange
5
atp-dependent sugar
4
transport complexity
4
complexity human
4
human erythrocytes
4
erythrocytes human
4
human erythrocyte
4

Similar Publications

Background: Diabetes is a modifiable risk factor for Alzheimer's disease, and GLUT4, an insulin-dependent transporter, plays a crucial role in insulin-resistant conditions and, consequently, in diabetes development. The study aimed to investigate the relationship between tau pathology and insulin resistance by quantifying GLUT4 expression and glucose concentration.

Method: Initially, SH-SY5Y cells underwent transfection with either a wild-type tau plasmid or a mutant tau plasmid.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Background: While disease-modifying treatments that reduce Aβ have been recently approved by the FDA, the identification of novel therapeutic targets and strategies that target underlying mechanisms to delay the AD development are still needed. Abnormal brain energy homeostasis and mitochondria dysfunction are observed early in AD. Therefore, the development of treatments to restore these defects could be beneficial.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Columbia University, New York, NY, USA.

Background: Genome-wide association studies (GWAS) have identified genetic loci that robustly associate with Alzheimer's Disease (AD), many of which are preferentially or exclusively expressed in innate immune cells. Among the identified AD risk genes is CD33: a transmembrane, sialic acid-binding protein expressed on the surface of myeloid cells including microglia, the innate immune cells of the CNS. The function of microglia is highly responsive to and regulated by metabolic changes, which allows them to rapidly change phenotype and maintain brain health.

View Article and Find Full Text PDF

Effect of empagliflozin on weight in patients with prediabetes and diabetes.

Sci Rep

January 2025

Health Services Management Research Center, Institute for Futures Studies in Health, Kerman University of Medical Sciences, Kerman, Iran.

The impact of blood glucose-lowering medications on weight has always been a topic of interest in the treatment of diabetic patients. This study investigates the effect of empagliflozin on weight in patients with prediabetes and type 2 diabetes. This quasi-experimental study was performed on patients with prediabetes or type 2 diabetes with an HbA1c level up to 1% higher than the treatment target, and not using other blood glucose-lowering medications.

View Article and Find Full Text PDF

Mitochondrial-cytochrome c oxidase II promotes glutaminolysis to sustain tumor cell survival upon glucose deprivation.

Nat Commun

January 2025

Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, China.

Glucose deprivation, a hallmark of the tumor microenvironment, compels tumor cells to seek alternative energy sources for survival and growth. Here, we show that glucose deprivation upregulates the expression of mitochondrial-cytochrome c oxidase II (MT-CO2), a subunit essential for the respiratory chain complex IV, in facilitating glutaminolysis and sustaining tumor cell survival. Mechanistically, glucose deprivation activates Ras signaling to enhance MT-CO2 transcription and inhibits IGF2BP3, an RNA-binding protein, to stabilize MT-CO2 mRNA.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!