The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Monounsaturated Fatty Acids Prevent the Deleterious Effects of Palmitate and High Glucose on Human Pancreatic β-Cell Turnover and Function
Open accessAbstract
Glucotoxicity and lipotoxicity contribute to the impaired β-cell function observed in type 2 diabetes. Here we examine the effect of saturated and monounsaturated fatty acids at different glucose concentrations on human β-cell turnover and secretory function. Exposure of cultured human islets to saturated fatty acid and/or to an elevated glucose concentration for 4 days increased β-cell DNA fragmentation and decreased β-cell proliferation. In contrast, the monounsaturated palmitoleic acid or oleic acid did not affect DNA fragmentation and induced β-cell proliferation. Moreover, each monounsaturated fatty acid prevented the deleterious effects of both palmitic acid and high glucose concentration. The cell-permeable ceramide analogue C2-ceramide mimicked both the palmitic acid-induced β-cell apoptosis and decrease in proliferation. Furthermore, the ceramide synthetase inhibitor fumonisin B1 blocked the deleterious effects of palmitic acid on β-cell turnover. In addition, palmitic acid decreased Bcl-2 expression and induced release of cytochrome c from the mitochondria into the cytosol, which was prevented by fumonisin B1 and by oleic acid. Finally, each monounsaturated fatty acid improved β-cell secretory function that was reduced by palmitic acid and by high glucose. Thus, in human islets, the saturated palmitic acid and elevated glucose concentration induce β-cell apoptosis, decrease β-cell proliferation, and impair β-cell function, which can be prevented by monounsaturated fatty acids. The deleterious effect of palmitic acid is mediated via formation of ceramide and activation of the apoptotic mitochondrial pathway, whereas Bcl-2 may contribute to the protective effect of monounsaturated fatty acids.
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Cites
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Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets
Maedler, K., Sergeev, P., Ris, F., Oberholzer, J., Joller-Jemelka, H. I., Spinas, G. A., Kaiser, N., Halban, P. A., & Donath, M. Y. (2017) · Journal of Clinical Investigation · doi:10.1172/jci92172 · Cited by 1,114
Self-citationGlucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets
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Cited by
Type 2 diabetes as an inflammatory disease
Donath, M. Y., & Shoelson, S. E. (2011) · Nature Reviews Immunology · doi:10.1038/nri2925 · Cited by 3,737
Self-citationIslet cell failure in type 2 diabetes
Prentki, M. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29103 · Cited by 1,690
The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives
Tsalamandris, S., Antonopoulos, A. S., Oikonomou, E., Papamikroulis, G.-A., Vogiatzi, G., Papaioannou, S., Deftereos, S., & Tousoulis, D. (2019) · European Cardiology Review · doi:10.15420/ecr.2018.33.1 · Cited by 1,381
Glucolipotoxicity: fuel excess and β-cell dysfunction
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Ceramides in insulin resistance and lipotoxicity
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Metadata
- Authors
- Maedler, K., Oberholzer, J., Bucher, P., Spinas, G. A., & Donath, M. Y.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2003-03-01
- Volume
- 52
- Issue
- 3
- Pages
- 726-733
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2128473384
- Cited by
- 549
- References
- 36
- FWCI
- 15.98
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Maedler, K., Oberholzer, J., Bucher, P., Spinas, G. A., & Donath, M. Y. (2003). Monounsaturated Fatty Acids Prevent the Deleterious Effects of Palmitate and High Glucose on Human Pancreatic β-Cell Turnover and Function. Diabetes. https://doi.org/10.2337/diabetes.52.3.726
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