Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury
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 <i>Caenorhabditis elegans</i> (<i>C. elegans&...
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MDPI AG
2021-05-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/11/5485 |
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| author | Karla Johanna Ruth Hoyer-Allo Martin Richard Späth Ruth Hanssen Marc Johnsen Susanne Brodesser Kathrin Kaufmann Katharina Kiefer Felix Carlo Koehler Heike Göbel Torsten Kubacki Franziska Grundmann Bernhard Schermer Jens Brüning Thomas Benzing Volker Burst Roman-Ulrich Müller |
| author_facet | Karla Johanna Ruth Hoyer-Allo Martin Richard Späth Ruth Hanssen Marc Johnsen Susanne Brodesser Kathrin Kaufmann Katharina Kiefer Felix Carlo Koehler Heike Göbel Torsten Kubacki Franziska Grundmann Bernhard Schermer Jens Brüning Thomas Benzing Volker Burst Roman-Ulrich Müller |
| author_sort | Karla Johanna Ruth Hoyer-Allo |
| collection | DOAJ |
| description | 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 <i>Caenorhabditis elegans</i> (<i>C. elegans</i>), 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 <i>C. elegans</i>, 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. |
| first_indexed | 2024-03-10T11:08:47Z |
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| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T11:08:47Z |
| publishDate | 2021-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-e0b7cfba1fad41dbaeed44db140aefb42023-11-21T20:58:02ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-05-012211548510.3390/ijms22115485Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney InjuryKarla Johanna Ruth Hoyer-Allo0Martin Richard Späth1Ruth Hanssen2Marc Johnsen3Susanne Brodesser4Kathrin Kaufmann5Katharina Kiefer6Felix Carlo Koehler7Heike Göbel8Torsten Kubacki9Franziska Grundmann10Bernhard Schermer11Jens Brüning12Thomas Benzing13Volker Burst14Roman-Ulrich Müller15Department II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyMax Planck Institute for Metabolism Research, Gleueler Str. 50, 50931 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Faculty of Medicine and University Hospital Cologne, Joseph-Stelzmann-Straße 26, 50931 Cologne, GermanyCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Faculty of Medicine and University Hospital Cologne, Joseph-Stelzmann-Straße 26, 50931 Cologne, GermanyCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Faculty of Medicine and University Hospital Cologne, Joseph-Stelzmann-Straße 26, 50931 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyInstitute of Pathology, University Hospital of Cologne, Kerpener Str. 37, 50937 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Faculty of Medicine and University Hospital Cologne, Joseph-Stelzmann-Straße 26, 50931 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Str. 37, 50937 Cologne, GermanyAcute 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 <i>Caenorhabditis elegans</i> (<i>C. elegans</i>), 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 <i>C. elegans</i>, 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.https://www.mdpi.com/1422-0067/22/11/5485acute kidney injuryischemia-reperfusion injurypreconditioningcaloric restrictionstress resistanceendocannabinoid |
| spellingShingle | Karla Johanna Ruth Hoyer-Allo Martin Richard Späth Ruth Hanssen Marc Johnsen Susanne Brodesser Kathrin Kaufmann Katharina Kiefer Felix Carlo Koehler Heike Göbel Torsten Kubacki Franziska Grundmann Bernhard Schermer Jens Brüning Thomas Benzing Volker Burst Roman-Ulrich Müller Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury International Journal of Molecular Sciences acute kidney injury ischemia-reperfusion injury preconditioning caloric restriction stress resistance endocannabinoid |
| title | Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury |
| title_full | Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury |
| title_fullStr | Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury |
| title_full_unstemmed | Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury |
| title_short | Modulation of Endocannabinoids by Caloric Restriction Is Conserved in Mice but Is Not Required for Protection from Acute Kidney Injury |
| title_sort | modulation of endocannabinoids by caloric restriction is conserved in mice but is not required for protection from acute kidney injury |
| topic | acute kidney injury ischemia-reperfusion injury preconditioning caloric restriction stress resistance endocannabinoid |
| url | https://www.mdpi.com/1422-0067/22/11/5485 |
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