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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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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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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