Obesity-related hypertension: Is there a role for selective leptin resistance?
Abstract
Obesity is a risk factor for cardiovascular diseases, in particular for hypertension. Serum leptin levels and sympathetic nerve activity are both increased in obesity. Leptin has been demonstrated to increase sympathetic nerve activity. Thus, leptin-dependent sympathoactivation might contribute to obesity-related hypertension. However, leptin resistance occurs in obesity. One possibility is that leptin resistance is selective to the metabolic effects of leptin, sparing its sympathoexcitatory actions. In this article, we review experimental evidence supporting the novel concept of selective leptin resistance. We also discuss the sympathetic actions of leptin that are relevant to blood pressure modulation and potential mechanisms of leptin resistance. Disruption of leptin intracellular signaling pathways and resistance of specific leptin-responsive neural networks provide theoretic models of selective leptin resistance. However, most information about leptin-sympathetic actions and leptin-resistance mechanisms derive from in vitro and animal studies. Future research in humans is widely awaited.
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Selective leptin resistance occurs in obesity.
“An intriguing aspect to consider with respect to the influence of leptin on the myocardium is the concept that selective leptin resistance occurs in obesity (60, 61, 222, 223).”
From Cardiac remodeling in obesity (2008) · cites this paper as [60]
In a high-fat induced model of obesity in mice, leptin resistance measured by STAT-3 activation was shown to be restricted to the arcuate nucleus of the hypothalamus, and this correlated with expression of the suppressor of leptin signaling SOCS-3.
“Indeed, using a high-fat induced model of obesity in mice, leptin resistance measured by STAT-3 activation was shown to be restricted to the arcuate nucleus of the hypothalamus (60, 194), and this correlated with expression of the suppressor of leptin signaling SOCS-3 (248).”
From Cardiac remodeling in obesity (2008) · cites this paper as [60]
Initial studies suggested that while the effects of leptin on satiety and energy metabolism were resistant, the sympathoexcitatory effects were maintained.
“Initial studies purporting this concept suggested that while the effects of leptin on satiety and energy metabolism were resistant, the sympathoexcitatory effects were maintained (60, 61, 222, 223, 290, 291).”
From Cardiac remodeling in obesity (2008) · cites this paper as [60]
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References 41 · Cited by 46
- Authors
- Correia, M. L. G., & Haynes, W. G.
- Affiliations
- University of Iowa (US)
- Venue
- Current Hypertension Reports
- Published
- 2004-05
- Volume
- 6
- Issue
- 3
- Pages
- 230-235
- ISSN
- 1522-6417 (ISSN-L)
- 1534-3111
- OpenAlex
- W2013611547
- Cited by
- 46
- References
- 41
- Citations by year
- 2024: 1 · 2023: 2 · 2021: 1 · 2020: 3 · 2018: 1 · 2016: 3 · 2013: 3 · 2012: 1
- FWCI
- 1.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Hypertension Reports (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- obesity, hypertension, leptin resistance, sympathetic activity, leptin, blood pressure regulation, leptin signaling, cardiovascular risk
- MeSH terms
- Blood Pressure, Drug Resistance, Humans, Hypertension, Nerve Net, Neural Pathways, Obesity, United States, Leptin
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