期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/ijms22115485
关键词
acute kidney injury; ischemia-reperfusion injury; preconditioning; caloric restriction; stress resistance; endocannabinoid; anandamide
资金
- Koeln Fortune program
- Cologne Clinician Scientist Program (CCSP)/Faculty of Medicine/University of Cologne
- German Research Foundation (DFG)/Faculty of Medicine, University of Cologne [FI 773/15-1]
- Koeln Fortune program/Faculty of Medicine/University of Cologne
- Nachwuchsgruppen NRW program of the Ministry of Science North Rhine Westfalia (MIWF)
- German Research Foundation [GR3932/2-1, SCHE1562/8, KFO329]
Research shows that caloric restriction (CR) can protect mice from renal ischemia-reperfusion injury (IRI) and significantly reduce AEA levels. However, in human trials, an increase in AEA levels was observed post-CR, unlike in mice and C. elegans. The study results suggest that CR modulates endocannabinoid levels in mice, but the CR-mediated renal protection is not dependent on this effect.
Acute kidney injury (AKI) is a frequent and critical complication in the clinical setting. In rodents, AKI can be effectively prevented through caloric restriction (CR), which has also been shown to increase lifespan in many species. In Caenorhabditis elegans (C. elegans), longevity studies revealed that a marked CR-induced reduction of endocannabinoids may be a key mechanism. Thus, we hypothesized that regulation of endocannabinoids, particularly arachidonoyl ethanolamide (AEA), might also play a role in CR-mediated protection from renal ischemia-reperfusion injury (IRI) in mammals including humans. In male C57Bl6J mice, CR significantly reduced renal IRI and led to a significant decrease of AEA. Supplementation of AEA to near-normal serum concentrations by repetitive intraperitoneal administration in CR mice, however, did not abrogate the protective effect of CR. We also analyzed serum samples taken before and after CR from patients of three different pilot trials of dietary interventions. In contrast to mice and C. elegans, we detected an increase of AEA. We conclude that endocannabinoid levels in mice are modulated by CR, but CR-mediated renal protection does not depend on this effect. Moreover, our results indicate that modulation of endocannabinoids by CR in humans may differ fundamentally from the effects in animal models.
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