ArticleScientific reports2016
A low-salt diet increases the expression of renal sirtuin 1 through activation of the ghrelin receptor in rats.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Sirtuins in kidney health and disease.Nature reviews. Nephrology · 2024Review
- Evaluation of glomerular sirtuin-1 and claudin-1 in the pathophysiology of nondiabetic focal segmental glomerulosclerosis.Scientific reports · 2023Article
- Oxidative Stress Induced by High Salt Diet-Possible Implications for Development and Clinical Manifestation of Cutaneous Inflammation and Endothelial Dysfunction inAntioxidants (Basel, Switzerland) · 2022Review
- Review
- Ghrelin Alleviates Intestinal Dysfunction in Sepsis Through the KLF4/MMP2 Regulatory Axis by Activating SIRT1.Frontiers in immunology · 2021Article
- Article
- Effects of Rikkunshito treatment on renal fibrosis/inflammation and body weight reduction in a unilateral ureteral obstruction model in mice.Scientific reports · 2020Article
- Acylated Ghrelin as a Multi-Targeted Therapy for Alzheimer's and Parkinson's Disease.Frontiers in neuroscience · 2020Review
- Effects of rikkunshito on renal fibrosis and inflammation in angiotensin II-infused mice.Scientific reports · 2019Article
- Ghrelin-mediated pathway in Apolipoprotein-E deficient mice: a survival system.American journal of translational research · 2019Article
- Combined Salt and Caloric Restrictions: Potential Adverse Outcomes.Journal of the American Heart Association · 2017Article
- Therapeutic Potential of Targeting the Ghrelin Pathway.International journal of molecular sciences · 2017Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that sirtuin 1 (Sirt1) is renoprotective; however, details regarding its distribution and functions in the kidney remain unknown. Here, we demonstrated that Sirt1 was mainly expressed in the tubulointerstitial cells of normal rat kidneys and was co-localized with aquaporin 2, indicating it may be involved in water/salt regulation. Renal Sirt1 expression increased in the non-glomerular cytoplasmic portion of the kidney after a 24-h fast, but no significant changes in Sirt1 expression occurred after water loading (50 mL/kg) or 24-h water deprivation. After consuming a low-salt (0.075%) or 60% calorie restriction diet for 7 days, Sirt1 expression in the rat kidney was significantly increased, whereas a high-salt (8%) diet did not change the level of Sirt1 expression. The low-salt diet also increased Sirt1 expression in the heart, muscle, brain, and fat tissues. The increased Sirt1 that was observed in rats on a low-salt diet was associated with increased ghrelin expression in the distal nephron, with both molecules exhibiting similar distribution patterns. An in vitro experiment suggested that ghrelin increases Sirt1 expression in cortical collecting duct cells by activating ghrelin receptors. Our study indicates that this 'ghrelin-Sirt1 system' may participate in regulating sodium reabsorption in the distal nephron.
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