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Toxicity Induced by Cytokines, Glucose, and Lipids Increase Apoptosis and Hamper Insulin Secretion in the 1.1E7 Beta Cell-Line

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URI: http://hdl.handle.net/10498/24711

DOI: 10.3390/ijms22052559

ISSN: 1422-0067

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2021_207.pdf (2.291Mb)
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Author/s
Diaz-Ganete, Antonia; Quiroga-de-Castro, Aranzazu; Mateos Bernal, Rosa MaríaAuthority UCA; Medina Prieto, Francisco; Segundo Iglesias, María del CarmenAuthority UCA; Lechuga Sancho, Alfonso MaríaAuthority UCA
Date
2021-03
Department
Biomedicina, Biotecnología y Salud Pública; Materno-Infantil y Radiología
Source
Int. J. Mol. Sci. 2021, 22(5), 2559
Abstract
Basic research on types 1 and 2 diabetes mellitus require early stage studies using beta cells or cell lines, ideally of human origin and with preserved insulin secretion in response to glucose. The 1.1E7 cells are a hybrid cell line resulting from the electrofusion of dispersed human islets and PANC-1 cells, capable of secreting insulin in response to glucose, but their survival and function under toxic conditions remains untested. This characterization is the purpose of the present study. We treated these cells with a cytokine mix, high glucose, palmitate, and the latter two combined. Under these conditions, we measured cell viability and apoptosis (MTT, Caspase Glo and TUNEL assays, as well as caspase-8 and -9 levels by Western blotting), endoplasmic reticulum stress markers (EIF2AK3, HSPA4, EIF2a, and HSPA5) by real-time PCR, and insulin secretion with a glucose challenge. All of these stimuli (i) induce apoptosis and ER stress markers expression, (ii) reduce mRNA amounts of 2-5 components of genes involved in the insulin secretory pathway, and (iii) abrogate the insulin release capability of 1.1E7 cells in response to glucose. The most pronounced effects were observed with cytokines and with palmitate and high glucose combined. This characterization may well serve as the starting point for those choosing this cell line for future basic research on certain aspects of diabetes.
Subjects
apoptosis; beta cell; cytokines; cytotoxicity; diabetes; glucotoxicity; lipotoxicity; mechanism
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  • Artículos Científicos [4845]
  • Articulos Científicos Biomedicina [213]
  • Artículos Científicos INIBICA [496]
  • Articulos Científicos Mat. Inf. Rad. [54]
Atribución 4.0 Internacional
This work is under a Creative Commons License Atribución 4.0 Internacional

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