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Cited by 319Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesBlood Pressure and Hypertension Studies

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Role of Selective Leptin Resistance in Diet-Induced Obesity Hypertension

Rahmouni, Kamal, Morgan, Donald A., Morgan, Gina M., Mark, Allyn L., Haynes, William G.·2005·Diabetes
DOI 10.2337/diabetes.54.7.2012
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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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Metadata

Authors
Rahmouni, K., Morgan, D. A., Morgan, G. M., Mark, A. L., & Haynes, W. G.
Affiliations
University of Iowa (US)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2005-07-01
Volume
54
Issue
7
Pages
2012-2018
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.54.7.2012
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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