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Repurposing anti-inflammasome NRTIs for improving insulin sensitivity and reducing type 2 diabetes development

  • Jayakrishna Ambati
  • , Joseph Magagnoli
  • , Hannah Leung
  • , Shao bin Wang
  • , Chris A. Andrews
  • , Dongxu Fu
  • , Akshat Pandey
  • , Srabani Sahu
  • , Siddharth Narendran
  • , Shuichiro Hirahara
  • , Shinichi Fukuda
  • , Jian Sun
  • , Lekha Pandya
  • , Meenakshi Ambati
  • , Felipe Pereira
  • , Akhil Varshney
  • , Tammy Cummings
  • , James W. Hardin
  • , Babatunde Edun
  • , Charles L. Bennett
  • Kameshwari Ambati, Benjamin J. Fowler, Nagaraj Kerur, Christian Röver, Norbert Leitinger, Brian C. Werner, Joshua D. Stein, S. Scott Sutton, Bradley D. Gelfand
  • University of Virginia
  • Columbia VA Health Care System
  • University of South Carolina
  • University of Tsukuba
  • Baystate Medical Center
  • University of Kentucky
  • University of Göttingen
  • University of Michigan, Ann Arbor

Research output: Contribution to journalArticlepeer-review

59 Scopus citations

Abstract

Innate immune signaling through the NLRP3 inflammasome is activated by multiple diabetes-related stressors, but whether targeting the inflammasome is beneficial for diabetes is still unclear. Nucleoside reverse-transcriptase inhibitors (NRTI), drugs approved to treat HIV-1 and hepatitis B infections, also block inflammasome activation. Here, we show, by analyzing five health insurance databases, that the adjusted risk of incident diabetes is 33% lower in patients with NRTI exposure among 128,861 patients with HIV-1 or hepatitis B (adjusted hazard ratio for NRTI exposure, 0.673; 95% confidence interval, 0.638 to 0.710; P < 0.0001; 95% prediction interval, 0.618 to 0.734). Meanwhile, an NRTI, lamivudine, improves insulin sensitivity and reduces inflammasome activation in diabetic and insulin resistance-induced human cells, as well as in mice fed with high-fat chow; mechanistically, inflammasome-activating short interspersed nuclear element (SINE) transcripts are elevated, whereas SINE-catabolizing DICER1 is reduced, in diabetic cells and mice. These data suggest the possibility of repurposing an approved class of drugs for prevention of diabetes.

Original languageEnglish
Article number4737
JournalNature Communications
Volume11
Issue number1
DOIs
StatePublished - Dec 1 2020

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