The DOI matches its Crossref record; 101 of the 101 references it cites were found in a registry or an index.
Leptin and hyperleptinemia - from friend to foe for cardiovascular function
Open accessAbstract
The obese gene product, leptin, plays a central role in food intake and energy metabolism. The physiological roles of leptin in human bodily function have been broadened over the past decade since leptin was first discovered in 1994. Evidence has suggested that leptin plays a specific role in the intricate cascade of cardiovascular events, in addition to its well-established metabolic effects. Leptin, a hormone linking adiposity and central nervous circuits to reduce appetite and enhance energy expenditure, has been shown to increase overall sympathetic nerve activity, facilitate glucose utilization and improve insulin sensitivity. In addition, leptin is capable of regulating cardiac and vascular contractility through a local nitric oxide-dependent mechanism. However, elevated plasma leptin levels or hyperleptinemia, have been demonstrated to correlate with hyperphagia, insulin resistance and other markers of the metabolic syndrome including obesity, hyperlipidemia and hypertension, independent of total adiposity. Elevated plasma leptin levels may be an independent risk factor for the development of cardiovascular disease. Although mechanisms leading to hyperleptinemia have not been well described, factors such as increased food intake and insulin resistance have been shown to rapidly enhance plasma leptin levels and subsequently tissue leptin resistance. These findings have prompted the speculation that leptin in the physiological range may serve as a physiological regulator of cardiovascular function whereas elevated plasma leptin levels may act as a pathophysiological trigger and/or marker for cardiovascular diseases due to tissue leptin resistance.
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“In general, the ob/ob mouse model is rather unique (plasma leptin levels are increased in almost all other obese rodent models and in humans, Ref. 297) and may not precisely reflect the alterations observed in human obesity.”
From Cardiac remodeling in obesity (2008) · cites this paper as [297]
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Cites
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“…activation of the sympathetic autonomic nervous system and impairment of endothelial function are the two pivotal phenotypical traits in obesity (Steinberg et al. 1996, Julius et al. 2000, Kuo et al. 2003), the cellular mechanisms responsible for sympathetic hyperactivity and endothelial…”
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Ortega, J. G., García-Muñoz, H., Ordóñez, A. S., & Contreras, B. C. S. (2022) · Figshare · doi:10.6084/m9.figshare.20962515
Obesity-Associated Cardiac Fibrosis: Mechanisms and Emerging Therapeutic Targets
Zhou, D., Tan, Y., Zhao, J., Wang, S., Wang, Z., Bai, M., Niu, X., & Zhang, Z. (2026) · Vascular Health and Risk Management · doi:10.2147/vhrm.s567568
Herrick, J. E. (2009) · VCU Scholars Compass (Virginia Commonwealth University) · doi:10.25772/08zr-f665
Metadata
- Authors
- Ren, J.
- Affiliations
- University of Wyoming (US)
- Corresponding author
- Ren, J
- ORCID
- Ren, J
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2004-04-01
- Volume
- 181
- Issue
- 1
- Pages
- 1-10
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2097827059
- Cited by
- 305
- References
- 97
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 8 · 2023: 6 · 2022: 12 · 2021: 12 · 2020: 6 · 2019: 10 · 2018: 6 · 2017: 7 · 2016: 10 · 2015: 14 · 2014: 16 · 2013: 18 · 2012: 19
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- American Heart Association
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- leptin, hyperleptinemia, cardiovascular disease, leptin resistance, insulin resistance, metabolic syndrome, obesity, hypertension, hyperlipidemia, sympathetic activity, insulin sensitivity, nitric oxide, cardiac contractility, vascular contractility, cardiovascular risk factors
- MeSH terms
- Appetite Regulation, Blood Glucose, Blood Pressure, Cardiovascular Diseases, Energy Metabolism, Heart Rate, Humans, Insulin, Obesity, Receptors, Cell Surface, Sympathetic Nervous System, Signal Transduction, Leptin, Receptors, Leptin
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