The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Leptin Effect on Endothelial Nitric Oxide Is Mediated Through Akt–Endothelial Nitric Oxide Synthase Phosphorylation Pathway
Abstract
Recent evidence suggests that besides its action on the central nervous system, leptin can modulate vascular tone through local mechanisms involving nitric oxide (NO) release. In this study, using a fluorescent probe for direct determination of NO, we demonstrated both in endothelial cells and in vessels that leptin is able to stimulate NO release. The effect of leptin on NO is abolished by erbstatin A, a Ca2+-independent tyrosine kinase inhibitor, whereas it is not influenced by calcium removal or by other protein phosphorylation inhibitors, such as genistein (an ATP-dependent tyrosine-kinase inhibitor) or wortmannin and LY294002 (two different phosphatidylinositol [PI] 3-kinase inhibitors). Accordingly, leptin-induced vasorelaxation in aortic rings was abolished only by erbstatin A. Furthermore, immunoblotting studies revealed that leptin evokes Akt phosphorylation, with a comparable time course in both endothelial cells and vessels. Also in this experimental system, the effect of leptin was abolished by erbstatin A and not by other inhibitors. Finally, a considerable increase in endothelial NO synthase (eNOS) phosphorylation in Ser1177 was found when vessels were treated with leptin. In conclusion, leptin induces NO production by activating a PI 3-kinase–independent Akt-eNOS phosphorylation pathway.
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Cites
Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation
Dimmeler, S., Fleming, I., Fisslthaler, B., Hermann, C., Busse, R., & Zeiher, A. M. (1999) · Nature · doi:10.1038/21224 · Cited by 3,591
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“This pathological condition is associated with a high incidence of hypertension and cardiovascular complications (2,3), which have in turn been linked to both the activation of the sympathetic nervous system (4) and the impairment of endothelial function (5), two pivotal phenotypical traits of obese subjects.”
Receptor-mediated regional sympathetic nerve activation by leptin.
Haynes, W. G., Morgan, D. A., Walsh, S. A., Mark, A. L., & Sivitz, W. I. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119532 · Cited by 979
Zeng, G., Nystrom, F. H., Ravichandran, L. V., Cong, L.-N., Kirby, M., Mostowski, H., & Quon, M. J. (2000) · Circulation · doi:10.1161/01.cir.101.13.1539 · Cited by 745
Overweight and Hypertension: A 2-Way Street?
Julius, S., Valentini, M., & Palatini, P. (2000) · Hypertension · doi:10.1161/01.hyp.35.3.807 · Cited by 253
Cited by
Kim, J.-A., Montagnani, M., Koh, K. K., & Quon, M. J. (2006) · Circulation · doi:10.1161/circulationaha.105.563213 · Cited by 1,652
Cardiovascular Actions of Insulin
Muniyappa, R., Montagnani, M., Koh, K. K., & Quon, M. J. (2007) · Endocrine Reviews · doi:10.1210/er.2007-0006 · Cited by 872
Regulation of endothelial and myocardial NO synthesis by multi-site eNOS phosphorylation
Mount, P. F., Kemp, B. E., & Power, D. A. (2007) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2006.05.023 · Cited by 498
eNOS, metabolic syndrome and cardiovascular disease
Huang, P. L. (2009) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2009.03.005 · Cited by 358
Leptin and hyperleptinemia - from friend to foe for cardiovascular function
Ren, J. (2004) · Journal of Endocrinology · doi:10.1677/joe.0.1810001 · Cited by 305
Metadata
- Authors
- Vecchione, C., Maffei, A., Colella, S., Aretini, A., Poulet, R., Frati, G., Gentile, M. T., Fratta, L., Trimarco, V., Trimarco, B., & Lembo, G.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2002-01-01
- Volume
- 51
- Issue
- 1
- Pages
- 168-173
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2147464692
- Cited by
- 330
- References
- 5
- FWCI
- 10.47
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Leptin Effect on Endothelial Nitric Oxide Is Mediated Through Akt–Endothelial Nitric Oxide Synthase Phosphorylation Pathway. https://app.cochat.ai/papers/10.2337/diabetes.51.1.168
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- Vecchione, C., Maffei, A., Colella, S., Aretini, A., Poulet, R., Frati, G., Gentile, M. T., Fratta, L., Trimarco, V., Trimarco, B., & Lembo, G. (2002). Leptin Effect on Endothelial Nitric Oxide Is Mediated Through Akt–Endothelial Nitric Oxide Synthase Phosphorylation Pathway. Diabetes. https://doi.org/10.2337/diabetes.51.1.168
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
