Physiological reports, 2021-03, Vol.9 (5), p.e14766-n/a
2021
Volltextzugriff (PDF)
Details
- Autor(en) / Beteiligte
- Titel
- Homoarginine ameliorates diabetic nephropathy independent of nitric oxide synthase‐3
- Ist Teil von
- Physiological reports, 2021-03, Vol.9 (5), p.e14766-n/a
- Ort / Verlag
- United States: John Wiley & Sons, Inc
- Erscheinungsjahr
- 2021
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Recently we showed that homoarginine supplementation confers kidney protection in diabetic mouse models. In this study we tested whether the protective effect of homoarginine is nitric oxide synthase‐3 (NOS3)‐independent in diabetic nephropathy (DN). Experiments were conducted in NOS3 deficient (NOS3−/−) mice and their wild type littermate using multiple low doses of vehicle or streptozotocin and treated with homoarginine via drinking water for 24 weeks. Homoarginine supplementation for 24 weeks in diabetic NOS3−/− mice significantly attenuated albuminuria, increased blood urea nitrogen, histopathological changes and kidney fibrosis, kidney fibrotic markers, and kidney macrophage recruitment compared with vehicle‐treated diabetic NOS3−/− mice. Furthermore, homoarginine supplementation restored kidney mitochondrial function following diabetes. Importantly, there were no significant changes in kidney NOS1 or NOS2 mRNA expression between all groups. In addition, homoarginine supplementation improved cardiac function and reduced cardiac fibrosis following diabetes. These data demonstrate that the protective effect of homoarginine is independent of NOS3, which will ultimately change our understanding of the mechanism(s) by which homoarginine induce renal and cardiac protection in DN. Homoarginine protective effect in DN could be mediated via improving mitochondrial function. Our results indicate that homoarginine mediates renal and cardiac protection in diabetic NOS3‐/‐ mice which will ultimately change our understanding of the mechanism(s) by which homoarginine ameliorate diabetic kidney injury. Homoarginine protective effect in diabetic nephropathy could be mediated via improving mitochondrial function.
- Sprache
- Englisch
- Identifikatoren
- eISSN: 2051-817XDOI: 10.14814/phy2.14766Titel-ID: cdi_doaj_primary_oai_doaj_org_article_f707223766d44a32a1abf424534cbdad
- Format
- –
- Schlagworte
- Albuminuria - metabolism, Animal models, Animals, Blood pressure, cardiac function, Cardiovascular disease, Diabetes, Diabetes mellitus, Diabetes Mellitus, Experimental - drug therapy, Diabetes Mellitus, Experimental - metabolism, Diabetic Nephropathies - drug therapy, Diabetic Nephropathies - metabolism, Diabetic nephropathy, Digital cameras, Drinking water, Fibrosis, Gene expression, Glucose, Heart, Heart failure, homoarginine, Homoarginine - metabolism, Homoarginine - pharmacology, Kidney - drug effects, Kidney - metabolism, Kidneys, Macrophages, Macrophages - metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, Mortality, Nephropathy, Nitric oxide, Nitric Oxide Synthase Type III - drug effects, Nitric-oxide synthase, NOS3, Original, Oxidative Stress - drug effects, Physiology, Plasma, Software, Streptozocin, Streptozocin - pharmacology, Supplements, Urea, Urine