ArticleThe Journal of biological chemistry2015
Insulin regulates nitric oxide production in the kidney collecting duct cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Understanding Insulin Actions Beyond Glycemic Control: A Narrative Review.Journal of clinical medicine · 2025Review
- Association of triglyceride glucose index with the risk of acute kidney injury in patients with coronary revascularization: a cohort study.Diabetology & metabolic syndrome · 2024Article
- Insulin and the kidneys: a contemporary view on the molecular basis.Frontiers in nephrology · 2023Review
- Hyperinsulinemia-induced microglial mitochondrial dynamic and metabolic alterations lead to neuroinflammationFrontiers in neuroscience · 2022Article
- Renal gluconeogenesis in insulin resistance: A culprit for hyperglycemia in diabetes.World journal of diabetes · 2021Review
- The market for amino acids: understanding supply and demand of substrate for more efficient milk protein synthesis.Journal of animal science and biotechnology · 2020Review
- Insulin receptors in the kidneys in health and disease.World journal of nephrology · 2019Review
- Chronic Insulin Infusion Down-Regulates Circulating and Urinary Nitric Oxide (NO) Levels Despite Molecular Changes in the Kidney Predicting Greater Endothelial NO Synthase Activity in Mice.International journal of molecular sciences · 2018Article
- Nitric oxide production by glomerular podocytes.Nitric oxide : biology and chemistry · 2018Article
- Insulin Resistance in Kidney Disease: Is There a Distinct Role Separate from That of Diabetes or Obesity?Cardiorenal medicine · 2017Review
- Hyperglycemia- and hyperinsulinemia-induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Activation of ATP-sensitive potassium channels facilitates the function of human endothelial colony-forming cells via CaJournal of cellular and molecular medicine · 2017Article
- Greater efficacy of atorvastatin versus a non-statin lipid-lowering agent against renal injury: potential role as a histone deacetylase inhibitor.Scientific reports · 2016Article
- Kidney tubules: intertubular, vascular, and glomerular cross-talk.Current opinion in nephrology and hypertension · 2016Review
- The association between PGC-1α and Alzheimer's disease.Anatomy & cell biology · 2016Review
- Urinary Exosomal microRNA-451-5p Is a Potential Early Biomarker of Diabetic Nephropathy in Rats.PloS one · 2016Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The kidney is an important organ for arterial blood pressure (BP) maintenance. Reduced NO generation in the kidney is associated with hypertension in insulin resistance. NO is a critical regulator of vascular tone; however, whether insulin regulates NO production in the renal inner medullary collecting duct (IMCD), the segment with the greatest enzymatic activity for NO production in kidney, is not clear. Using an NO-sensitive 4-amino-5-methylamino-2',7'-difluorofluorescein (DAF-FM) fluorescent dye, we found that insulin increased NO production in mouse IMCD cells (mIMCD) in a time- and dose-dependent manner. A concomitant dose-dependent increase in the NO metabolite (NOx) was also observed in the medium from insulin-stimulated cells. NO production peaked in mIMCD cells at a dose of 100 nm insulin with simultaneously increased NOx levels in the medium. At this dose, insulin significantly increased p-eNOS(Ser1177) levels in mIMCD cells. Pretreatment of cells with a PI 3-kinase inhibitor or insulin receptor silencing with RNA interference abolished these effects of insulin, whereas insulin-like growth factor-1 receptor (IGF-1R) silencing had no effect. We also showed that chronic insulin infusion to normal C57BL/6J mice resulted in increased endothelial NOS (eNOS) protein levels and NO production in the inner medulla. However, insulin-infused IRKO mice, with targeted deletion of insulin receptor from tubule epithelial cells of the kidney, had ∼50% reduced eNOS protein levels in their inner medulla along with a significant rise in BP relative to WT littermates. We have previously reported increased baseline BP and reduced urine NOx in IRKO mice. Thus, reduced insulin receptor signaling in IMCD could contribute to hypertension in the insulin-resistant state.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.