DOI: https://doi.org/10.14710/jbtr.v9i3.19644

The Effect of Increased Glucose Induction on GSH Levels in Insulin Gaussia Luciferase (iGL) Cells Derived from Rat Pancreatic Beta Cells

Faculty of Medicine, Universitas Muhammadiyah Prof. DR. HAMKA, Indonesia

Received: 26 Jul 2023; Revised: 24 Dec 2023; Accepted: 7 Dec 2023; Available online: 31 Dec 2023; Published: 31 Dec 2023.
Open Access Copyright (c) 2023 Journal of Biomedicine and Translational Research
Creative Commons License This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.

Citation Format:
Abstract

Background: Prolonged hyperglycaemia can make the pancreatic beta cells work harder and cause fatigue. When this happens, it can trigger oxidative stress reactions, which can produce free radical compounds that can damage pancreatic beta cells. The body compensates by activating protective mechanisms such as the production of antioxidant compounds to reduce the levels of free radicals in the cells. One such compound is glutathione (GSH). Insulin Gaussia Luciferase (iGL) cells are a cell line derived from rat pancreatic β (beta) cells. These cells can be used as a model of oxidative stress in hyperglycaemia to measure GSH levels and there are no studies using iGL cells to measure GSH levels. Therefore, in this study, the iGL cells are used as the object of research.

Objective: To investigate the effect of GSH levels on glucose toxicity condition through in vitro experiments on iGL cells.

Methods: The study used 5 different glucose concentrations of 11, 16.5, 22, 33, and 44 mM with the addition of iGL cell growth medium exposed for 7 days. We measured the amount of intracellular GSH using a colourimetric method at a wavelength of 405 nm. The analysis used in this study was a one-way ANOVA test. Differences between groups were tested using SPSS.

Results: The results of this study showed that there was an increasing trend in total GSH levels on the third and seventh day.

Conclusion: there was a daily decrease in GSH/cell in the iGL sample cells exposed to different concentrations of glucose for 7 days. This can be due to an increase in the oxidative stress reactions in the cells, which can lead to a decrease in the levels of antioxidants.

Fulltext View|Download
Keywords: Colorimetric method, GSH, Hyperglycaemia, iGL cells, Oxidative stress.

Article Metrics:

Article Info
Section: Original Research Articles
Language : EN
Recent articles
Comparison of SARS-CoV-2 Variant Screening and Whole Genome Sequencing at an Indonesian Tertiary Hospitals The Effect of Increased Glucose Induction on GSH Levels in Insulin Gaussia Luciferase (iGL) Cells Derived from Rat Pancreatic Beta Cells Analysis Of Clerodendrum inerme Plant Compounds as Anti Diabetes Mellitus Through Network Pharmacology Approach Recalcitrant Incomplete Secukinumab Administration in a Psoriasis Patient Exploring Systemic Lupus Erythematosus Pathogenesis through Animal Models: A Systematic Review of Humanized and Pristane-Induced Lupus Mice More recent articles
  1. Alterzon SB et al. Nrf2: The Master and Captain of Beta Cell Fate. Trends Endocrinol Metab. 2021; DOI: 10.1016/j.tem.2020.11.002
  2. American Diabetes Association. Diagnosis and Classification of Diabetes Mellitus. 2013; Available from: https://www.diabetesjournals.org/care/issue/37/Supplement_1
  3. Cosmo Bio Co. iGL Cell Line. 2020
  4. Flohé L. GLUTHATHIONE. 2018; DOI: 10.1201/9781351261760
  5. International Diabetes Federation. IDF Diabetes ATLAS. 2020. Available from: https://www.diabetesatlas.org/ atlas/nineth-edition
  6. Kaneto H, Matsuoka TA. Role of pancreatic transcription factors in maintenance of mature β-cell function. Vol. 16, International Journal of Molecular Sciences. MDPI AG; 2015. p. 6281–97. DOI: 10.3390/ijms16036281
  7. Lv L, Wang X, Shen J, Cao Y, Zhang Q. MiR-574-3p inhibits glucose toxicity-induced pancreatic β-cell dysfunction by suppressing PRMT1. Diabetol Metab Syndr. 2022 Dec 1;14(1). DOI: 10.1186/s13098-022-00869-y
  8. My Biosource. Reduced Glutathione (GSH) Colorimetric Assay Kit. 2018
  9. Ningsih SS, AR, SEN, LE, YT, & SWS. Evaluation of morphology and viability of spheroid derived from Insulin-GLase cell line: A model system to understand Type 2 Diabetes Mellitus. Journal of Experimental and Clinical Medicine (Turkey). 2021;38(3):211–5. DOI: 10.52142/omujecm.38.3.1
  10. Oyehihi AB AA. Antioxidant Strategies in the Management of Diabetic Neuropathy. . Biomed Res Int. 2015; DOI: 10.1155/2015/515042
  11. Paul RR. DeGroot`s Endocrinology Basic Science and Clinical Practice. 8th ed. Elsevier; 2022. Available from: https://www.books.google.co.id/books/about/Degroot_s_Endocrinology
  12. Qiang Ma. Role of Nrf2 in Oxidative Stress and Toxicity. 2013; DOI: 10.1146/annurev-pharmtox-011112-140320
  13. Robert C. Stanton. Glucose-6-Phosphate Dehydrogenase, NADPH, and Cell Survival. 2012; DOI: 10.1002/iub.1017
  14. Shen CY, Lu CH, Wu CH, Li KJ, Kuo YM, Hsieh SC, et al. The development of maillard reaction, and advanced glycation end product (Age)-receptor for age (rage) signaling inhibitors as novel therapeutic strategies for patients with age-related diseases. Vol. 25, Molecules. MDPI AG; 2020. DOI: 10.3390/molecules25235591
  15. Sherwood L. Human Physiology From Cells to Systems 9th Editions. 2016. Available from: https://www.books.google.co.id/books.id
  16. Suzuki T, KT, & IS. Quantitative visualization of synchronized insulin secretion from 3D-cultured cells. Biochemical and Biophysical Research Communications, . 2017;486(4):886–92. DOI: 10.1016/j.bbrc.2017.03.105
  17. Tatsuo Tomita. Apoptosis in pancreatic β-islet cells in Type 2 diabetes. Journal of the Association of Basic Medical Sciences. 2016;16. DOI: 10.17305/bjbms.2016.919
  18. Usha Rani MSASSLJAA and SA. Evaluation of Use of RPMI Medium to Preserve Cell Morphology for Pleural/Peritoneal Fluid Cytology. J Cytol. 2022 Feb;39. DOI: 10.4103/joc.joc_130_21
  19. Vicent Ribas CGR and JCFC. Gluthathione and Mitochondria. Front Pharmacol. 2014;5: DOI: 10.3389/fphar.2014.00151
  20. WHO. Classification of Diabetes Mellitus 2019. 2019; Available from: https://www.who.int/publications/i/item/classification-of-diabetes-mellitus

Last update:

No citation recorded.

Last update:

No citation recorded.