Global Analysis of Metabolic Fluxes of Glucose and Glutamine in INS‑1 Cells Exposed to Arsenite Using ¹³C‑Isotopic Tracers.
5 affiliations
- 1School of Environmental Science and Engineering, School of Life and Health Sciences, Hainan University, Haikou 570228, China.
- 2State Key Laboratory of Biocontrol, School of Life Sciences, School of Marine Sciences, Sun Yat-sen University, Guangzhou 510275, China.
- 3Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
- 4Department of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China.
- 5Jiangmen Key Laboratory of Synthetic Chemistry and Cleaner Production, School of Environmental and Chemical Engineering, Wuyi University, Jiangmen 529020, China.
Abstract
Human exposure to arsenic has been reported to induce metabolic disorders in pancreatic β-cells. However, metabolic fluxes of essential carbon sources in pancreatic β-cells under arsenic exposure were not quantitatively characterized. In this study, ¹³C-labeled glucose and glutamine were used as the tracers to examine their fates in INS-1 832/13 cells treated with arsenite (iAsIII). INS-1 832/13 cells exposed to three concentrations of iAsIII (0.05, 0.5, and 1.0 μg/mL) maintained at least 80.0% of cell viability in comparison to the controls. Glucose uptake of INS-1 832/13 cells exposed to 1.0 μg/mL iAsIII was approximately 2 times higher than that of the controls. Accordingly, glucose was also accumulated in the iAsIII-treated INS-1 832/13 cells. The activities of glucose-derived pathways in INS-1 832/13 cells, including glycolysis, tricarboxylic acid (TCA) cycle, and pentose phosphate pathway (PPP), were consistently enhanced by iAsIII. However, mitochondrial respiratory indexes of INS-1 832/13 cells, including oxygen consumption rate (OCR), ATP-linked OCR, basal OCR, maximal respiration, and spare respiratory capacity, were considerably suppressed by iAsIII. Inhibitive effects of iAsIII on metabolic pathway activities of glutamine were observed. Collectively, our results suggest that iAsIII exposure can induce metabolic reprogramming involved with glucose and glutamine in INS-1 832/13 cells.
Related
- Mitochondrial metabolic reprogramming by a glutamine antagonist radioenhancer conjugate drives pyroptosis and antitumor immunity
- Post-Exposure 3-Methyladenine Is Associated with Lower Indices of Hepatic Injury and Fibrotic Remodeling After Chronic Sodium Arsenite Exposure in Mice.
- Copper(I)-catalyzed enantioselective Truce-Smiles rearrangement to access glutamine motifs bearing 1,3-nonadjacent stereocenters
- Effects of Pretreatment on the Isotopic Composition of Structural Carbonate in Ray‐Finned Fish Teeth
- High-Performance Chemiresistive Humidity Sensing and Quantum Isotopic Differentiation with Single Crystals of a Conductive MOF Hosting Electron Spin Qubits
BibTeX
@article{zhang2026global,
title = {{Global Analysis of Metabolic Fluxes of Glucose and Glutamine in INS‑1 Cells Exposed to Arsenite Using ¹³C‑Isotopic Tracers.}},
author = {Ruijia Zhang and Liangyu Chen and Yingshi Lin and Wenhua Lu and Yizheng Li and Yangyang An and Qihong Yan and Xubin Yang and Tiangang Luan and Baowei Chen},
journal = {Environment \& health (Washington, D.C.)},
year = {2026},
month = may,
doi = {10.1021/envhealth.5c00614},
url = {https://europepmc.org/article/MED/42903685},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Global Analysis of Metabolic Fluxes of Glucose and Glutamine in INS‑1 Cells Exposed to Arsenite Using ¹³C‑Isotopic Tracers.
AU - Ruijia Zhang
AU - Liangyu Chen
AU - Yingshi Lin
AU - Wenhua Lu
AU - Yizheng Li
AU - Yangyang An
AU - Qihong Yan
AU - Xubin Yang
AU - Tiangang Luan
AU - Baowei Chen
PY - 2026
DA - 2026/05/22
JO - Environment & health (Washington, D.C.)
DO - 10.1021/envhealth.5c00614
UR - https://europepmc.org/article/MED/42903685
AB - Human exposure to arsenic has been reported to induce metabolic disorders in pancreatic β-cells. However, metabolic fluxes of essential carbon sources in pancreatic β-cells under arsenic exposure were not quantitatively characterized. In this study, ¹³C-labeled glucose and glutamine were used as the tracers to examine their fates in INS-1 832/13 cells treated with arsenite (iAsIII). INS-1 832/13 cells exposed to three concentrations of iAsIII (0.05, 0.5, and 1.0 μg/mL) maintained at least 80.0% of cell viability in comparison to the controls. Glucose uptake of INS-1 832/13 cells exposed to 1.0 μg/mL iAsIII was approximately 2 times higher than that of the controls. Accordingly, glucose was also accumulated in the iAsIII-treated INS-1 832/13 cells. The activities of glucose-derived pathways in INS-1 832/13 cells, including glycolysis, tricarboxylic acid (TCA) cycle, and pentose phosphate pathway (PPP), were consistently enhanced by iAsIII. However, mitochondrial respiratory indexes of INS-1 832/13 cells, including oxygen consumption rate (OCR), ATP-linked OCR, basal OCR, maximal respiration, and spare respiratory capacity, were considerably suppressed by iAsIII. Inhibitive effects of iAsIII on metabolic pathway activities of glutamine were observed. Collectively, our results suggest that iAsIII exposure can induce metabolic reprogramming involved with glucose and glutamine in INS-1 832/13 cells.
SN - 2833-8278
ER -