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Role of Selective Leptin Resistance in Diet-Induced Obesity Hypertension
Abstract
Leptin is an adipocyte-derived hormone that plays a key role in the regulation of body weight through its actions on appetite and metabolism. Leptin also increases sympathetic nerve activity (SNA) and blood pressure. We tested the hypothesis that diet-induced obesity is associated with resistance to the metabolic actions of leptin but preservation of its renal SNA and arterial pressure effects, leading to hypertension. Mice were fed a high-fat diet for 10 weeks to induce moderate obesity. The decrease in food intake and body weight induced by intraperitoneal or intracerebroventricular leptin was significantly attenuated in the obese mice. Regional SNA responses to leptin were differentially altered in diet-induced obese mice. Renal SNA response to leptin was preserved, whereas lumbar and brown adipose tissue SNA responses were attenuated in obese mice. Radiotelemetric arterial pressure was ∼10 mmHg higher in obese mice. Furthermore, the increase in arterial pressure in response to long-term (12 days) leptin treatment was preserved in obese mice. Thus, mice with diet-induced obesity exhibit circulating hyperleptinemia and resistance to the metabolic actions of leptin. However, there is preservation of the renal sympathetic and arterial pressure responses to leptin, which represent a potential mechanism for the adverse cardiovascular consequences of obesity.
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“Although the suppressive effects of leptin on food intake are blunted in obesity, its acute stimulatory actions on RSNA seem to be preserved, suggesting selective leptin resistance126,136.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [136]
In the citing paper
“In obese mice, leptin’s anorexic effects were blunted whereas the acute effects to increase RSNA were preserved104.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [104]
In the citing paper
“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 [291]
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Metadata
- Authors
- Rahmouni, K., Morgan, D. A., Morgan, G. M., Mark, A. L., & Haynes, W. G.
- Affiliations
- University of Iowa (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-07-01
- Volume
- 54
- Issue
- 7
- Pages
- 2012-2018
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2012264731
- Cited by
- 319
- References
- 31
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 9 · 2019: 6 · 2018: 7 · 2017: 19 · 2016: 14 · 2015: 16 · 2014: 16 · 2013: 25 · 2012: 19
- FWCI
- 9.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health (5p50hl044546-05)
- National Heart, Lung, and Blood Institute (HL-14388, HL-44546, P01HL014388)
- 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 › Blood Pressure and Hypertension Studies
- Keywords
- leptin resistance, diet-induced obesity, hypertension, sympathetic activity, renal sympathetic nerve activity, arterial pressure, high-fat diet, hyperleptinemia, brown adipose tissue
- MeSH terms
- Animals, Blood Pressure, Adipose Tissue, Brown, Dietary Fats, Disease Models, Animal, Drug Resistance, Hypertension, Injections, Intraventricular, Male, Mice, Inbred C57BL, Obesity, Leptin, Mice
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