Uric acid induces oxidative stress and growth inhibition by activating adenosine monophosphate-activated protein kinase and extracellular signal-regulated kinase signal pathways in pancreatic β cells
Molecular and Cellular Endocrinology, ISSN: 0303-7207, Vol: 375, Issue: 1, Page: 89-96
2013
- 106Citations
- 62Captures
- 1Mentions
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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
- Citations106
- Citation Indexes106
- 106
- CrossRef73
- Captures62
- Readers62
- 62
- Mentions1
- News Mentions1
- News1
Most Recent News
The Management of Diabetes with Hyperuricemia: Can We Hit Two Birds with One Stone?
Introduction A large body of recent evidence suggests that hyperuricemia (HU) may play a role in the development and pathogenesis of a number of metabolic,
Article Description
Hyperuricaemia is a disorder of purine metabolism, and is strongly associated with insulin resistance and abnormal glucose metabolism. As the producer of insulin, pancreatic β cells might be affected by elevated serum uric acid levels and contribute to the disregulated glucose metabolism. In this study, we investigated the effect of high uric acid on rat pancreatic β cell function. Under high uric acid condition, proliferation of pancreatic β cells was inhibited, production of reactive oxygen species increased, and glucose stimulated insulin secretion was also compromised. Further examination on signal transduction pathways revealed that uric acid-induced ROS is involved in the activation of adenosine monophosphate-activated protein kinase (AMPK), and extracellular signal-regulated kinase (ERK). Pharmacological inhibition of ERK activation rescued β cells from growth inhibition. More importantly, activation of ERK induced by uric acid is significantly diminished by AMPK inhibitor, indicating ERK as a downstream target of AMPK in response to high uric acid condition. We also investigated the transportation channel for uric acid into pancreatic β cells. While major urate transporter URAT1 is not expressed in β cells, organic anion transporter (OAT) inhibitor successfully blocked the activation of ERK by uric acid. Our data indicate that high uric acid levels induce oxidative damage and inhibit growth of rat pancreatic β cells by activating the AMPK and ERK signal pathways. Hyperuricemia may contribute to abnormal glucose metabolism by causing oxidative damage and function inhibition of pancreatic β cells.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0303720713002086; http://dx.doi.org/10.1016/j.mce.2013.04.027; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84878932271&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/23707617; https://linkinghub.elsevier.com/retrieve/pii/S0303720713002086; https://dx.doi.org/10.1016/j.mce.2013.04.027
Elsevier BV
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