Prolonged exposure to free fatty acids has cytostatic and pro-apoptotic effects on human pancreatic islets: evidence that beta-cell death is caspase mediated, partially dependent on ceramide pathway, and Bcl-2 regulated - PubMed (original) (raw)
. 2002 May;51(5):1437-42.
doi: 10.2337/diabetes.51.5.1437.
Francesco Dotta, Lorella Marselli, Silvia Del Guerra, Matilde Masini, Carmela Santangelo, Giovanni Patané, Ugo Boggi, Salvatore Piro, Marcello Anello, Ettore Bergamini, Franco Mosca, Umberto Di Mario, Stefano Del Prato, Piero Marchetti
Affiliations
- PMID: 11978640
- DOI: 10.2337/diabetes.51.5.1437
Prolonged exposure to free fatty acids has cytostatic and pro-apoptotic effects on human pancreatic islets: evidence that beta-cell death is caspase mediated, partially dependent on ceramide pathway, and Bcl-2 regulated
Roberto Lupi et al. Diabetes. 2002 May.
Abstract
In an effort to better understand the phenomenon of lipotoxicity in human beta-cells, we evaluated the effects of 48-h preculture with 1.0 or 2.0 mmol/l free fatty acid (FFA) (2:1 oleate to palmitate) on the function and survival of isolated human islets and investigated some of the possible mechanisms. Compared with control islets, triglyceride content was significantly increased and insulin content and glucose-stimulated insulin release were significantly reduced in islets precultured with increased FFA concentrations. These changes were accompanied by a significant reduction of glucose utilization and oxidation. By cell death detection techniques, it was observed that exposure to FFAs induced a significant increase of the amount of dead cells. Electron microscopy showed the involvement of beta-cells, with morphological appearance compatible with the presence of apoptotic phenomena. FFA-induced islet cell death was blocked by inhibition of upstream caspases and partially prevented by inhibiton of ceramide synthesis or serine protease activity, whereas inhibition of nitric oxide synthesis had no effect. RT-PCR studies revealed no major change of iNOS and Bax mRNA expression and a marked decrease of Bcl-2 mRNA expression in the islets cultured with FFA. Thus, prolonged exposure to FFAs has cytostatic and pro-apoptotic effects on human pancreatic beta-cells. The cytostatic action is likely to be due to the FFA-induced reduction of intraislet glucose metabolism, and the proapoptotic effects are mostly caspase mediated, partially dependent on ceramide pathway, and possibly Bcl-2 regulated.
Similar articles
- Chronic exposure to free fatty acids or high glucose induces apoptosis in rat pancreatic islets: possible role of oxidative stress.
Piro S, Anello M, Di Pietro C, Lizzio MN, Patanè G, Rabuazzo AM, Vigneri R, Purrello M, Purrello F. Piro S, et al. Metabolism. 2002 Oct;51(10):1340-7. doi: 10.1053/meta.2002.35200. Metabolism. 2002. PMID: 12370856 - The role of peripheral benzodiazepine receptors on the function and survival of isolated human pancreatic islets.
Marselli L, Trincavelli L, Santangelo C, Lupi R, Del Guerra S, Boggi U, Falleni A, Gremigni V, Mosca F, Martini C, Dotta F, Di Mario U, Del Prato S, Marchetti P. Marselli L, et al. Eur J Endocrinol. 2004 Aug;151(2):207-14. doi: 10.1530/eje.0.1510207. Eur J Endocrinol. 2004. PMID: 15296476 - Metformin restores insulin secretion altered by chronic exposure to free fatty acids or high glucose: a direct metformin effect on pancreatic beta-cells.
Patanè G, Piro S, Rabuazzo AM, Anello M, Vigneri R, Purrello F. Patanè G, et al. Diabetes. 2000 May;49(5):735-40. doi: 10.2337/diabetes.49.5.735. Diabetes. 2000. PMID: 10905481 - Pleiotropic effects of fatty acids on pancreatic beta-cells.
Haber EP, Ximenes HM, Procópio J, Carvalho CR, Curi R, Carpinelli AR. Haber EP, et al. J Cell Physiol. 2003 Jan;194(1):1-12. doi: 10.1002/jcp.10187. J Cell Physiol. 2003. PMID: 12447984 Review. - Lipotoxicity in the pathogenesis of obesity-dependent NIDDM. Genetic and clinical implications.
Unger RH. Unger RH. Diabetes. 1995 Aug;44(8):863-70. doi: 10.2337/diab.44.8.863. Diabetes. 1995. PMID: 7621989 Review.
Cited by
- Mechanism of Obesity-Related Lipotoxicity and Clinical Perspective.
Engin AB. Engin AB. Adv Exp Med Biol. 2024;1460:131-166. doi: 10.1007/978-3-031-63657-8_5. Adv Exp Med Biol. 2024. PMID: 39287851 Review. - Association of common single-nucleotide polymorphism of HHEX with type 2 diabetes mellitus.
Hasti S, Mirfeizi M, Afshari M, Hasanzad M, Moghadam FA, Aghaei Meybodi HR. Hasti S, et al. J Diabetes Metab Disord. 2024 Apr 18;23(1):1183-1187. doi: 10.1007/s40200-024-01407-5. eCollection 2024 Jun. J Diabetes Metab Disord. 2024. PMID: 38932910 - Mitochondrial Dysfunction, Oxidative Stress, and Inter-Organ Miscommunications in T2D Progression.
Veluthakal R, Esparza D, Hoolachan JM, Balakrishnan R, Ahn M, Oh E, Jayasena CS, Thurmond DC. Veluthakal R, et al. Int J Mol Sci. 2024 Jan 25;25(3):1504. doi: 10.3390/ijms25031504. Int J Mol Sci. 2024. PMID: 38338783 Free PMC article. Review. - Beta-cell function in type 2 diabetes (T2DM): Can it be preserved or enhanced?
Sayyed Kassem L, Rajpal A, Barreiro MV, Ismail-Beigi F. Sayyed Kassem L, et al. J Diabetes. 2023 Oct;15(10):817-837. doi: 10.1111/1753-0407.13446. Epub 2023 Jul 31. J Diabetes. 2023. PMID: 37522521 Free PMC article. Review. - Type 2 Diabetes and Alzheimer's Disease: The Emerging Role of Cellular Lipotoxicity.
Marrano N, Biondi G, Borrelli A, Rella M, Zambetta T, Di Gioia L, Caporusso M, Logroscino G, Perrini S, Giorgino F, Natalicchio A. Marrano N, et al. Biomolecules. 2023 Jan 16;13(1):183. doi: 10.3390/biom13010183. Biomolecules. 2023. PMID: 36671568 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials