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

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
Open this paper in CoChat — free account

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.

Integrity signals

Registry

Crossref · 10.2337/diabetes.54.7.2012

Cites

32 of 32 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Although the suppressive effects of leptin on food intake are blunted in obesity, its acute stimulatory actions on renal sympathetic nerve activity seem to be preserved, suggesting selective leptin resistance.

    “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 obese mice, leptin's anorexic effects were blunted whereas the acute effects to increase RSNA were preserved.

    “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]

  • 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 [291]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

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 › Epidemiology › 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

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 ›

Are you an author, or do you see a problem with this page? Request a review