Insights in diabetes: Molecular mechanisms-Protectin DX, an anti-inflammatory and a stimulator of inflammation resolution metabolite of docosahexaenoic acid, protects against the development of streptozotocin-induced type 1 and type 2 diabetes mellitus in male Swiss albino mice
Frontiers in Endocrinology, ISSN: 1664-2392, Vol: 13, Page: 1053879
2023
- 11Citations
- 9Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations11
- Citation Indexes11
- 11
- Captures9
- Readers9
Article Description
Our previous studies revealed that certain endogenous low molecular weight lipids have potent anti-diabetic actions. Of all, arachidonic acid (AA) and its anti-inflammatory and inflammation resolving metabolite lipoxin A4 (LXA4) are the most potent anti-diabetic molecules. Similar anti-diabetic action is also shown by resolvins. In our efforts to identify other similar lipid based anti-diabetic molecules, we investigated potential anti-diabetic action of protectin DX that also has anti-inflammatory and inducer of inflammation resolution action(s) like LXA4. Protectin DX {10(S),17(S)-dihydroxy-4Z,7Z,11E,13Z,15E,19Z-docosahexaenoic acid, also called as 10(S),17(S)-DiHDoHE)} prevented the development of streptozotocin-induced type 1 and type 2 diabetes mellitus in Swiss male albino mice. Protectin DX showed potent anti-inflammatory, antioxidant and anti-apoptotic actions that could explain its anti-diabetic action. In view of these beneficial actions, efforts need to be developed to exploit PDX and other similar compounds as potential anti-diabetic molecule in humans.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85147659711&origin=inward; http://dx.doi.org/10.3389/fendo.2022.1053879; http://www.ncbi.nlm.nih.gov/pubmed/36778598; https://www.frontiersin.org/articles/10.3389/fendo.2022.1053879/full; https://dx.doi.org/10.3389/fendo.2022.1053879; https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2022.1053879/full
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