Nature communications · 2020
Repurposing anti-inflammasome NRTIs for improving insulin sensitivity and reducing type 2 diabetes development.
СтатьяМетаанализПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ambati Jayakrishna, Magagnoli Joseph, Leung Hannah, Wang Shao-Bin, Andrews Chris A, Fu Dongxu, Pandey Akshat, Sahu Srabani, Narendran Siddharth, Hirahara Shuichiro, Fukuda Shinichi, Sun Jian, Pandya Lekha, Ambati Meenakshi, Pereira Felipe, Varshney Akhil, Cummings Tammy, Hardin James W, Edun Babatunde, Bennett Charles L, Ambati Kameshwari, Fowler Benjamin J, Kerur Nagaraj, Röver Christian, Leitinger Norbert, Werner Brian C, Stein Joshua D, Sutton S Scott, Gelfand Bradley D
Аннотация
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.