Evidence map›Paper›PMID 26628674›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Regulation of Blood Pressure, Appetite, and Glucose by Leptin After Inactivation of Insulin Receptor Substrate 2 Signaling in the Entire Brain or in Proopiomelanocortin Neurons.

Jussara M do Carmo, Alexandre A da Silva, Zhen Wang, Nathan J Freeman, Ammar J Alsheik, Ahmad Adi, John E Hall

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025
    Review
  3. Review
  4. OBESITY & HYPERTENSION - 'TWO PEAS IN A POD'.Annals of Ibadan postgraduate medicine · 2024
    Article
  5. Transient receptor potential cation channel 6 deficiency leads to increased body weight and metabolic dysfunction.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  6. Review
  7. Article
  8. Review
  9. Impact of leptin deficiency compared with neuronal-specific leptin receptor deletion on cardiometabolic regulation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  10. Review
  11. Role of SOCS3 in POMC neurons in metabolic and cardiovascular regulation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Role of autonomic nervous system in chronic CNS-mediated antidiabetic action of leptin.American journal of physiology. Endocrinology and metabolism · 2017
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Jussara M do CarmoFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson. jdocarmo@umc.edu.
Alexandre A da SilvaFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson.
Zhen WangFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson.
Nathan J FreemanFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson.
Ammar J AlsheikFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson.
Ahmad AdiFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson.
John E HallFrom the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
NHLBI NIH HHS P01 HL051971NHLBI NIH HHS P01 HL-51971NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P20GM104357
6 · The paper itself

Abstract

Insulin receptor substrate 2 (IRS2) is one of the 3 major leptin receptor signaling pathways, but its role in mediating the chronic effects of leptin on blood pressure, food intake, and glucose regulation is unclear. We tested whether genetic inactivation of IRS2 in the entire brain (IRS2/Nestin-cre mice) or specifically in proopiomelanocortin (POMC) neurons (IRS2/POMC-cre mice) attenuates the chronic cardiovascular, metabolic, and antidiabetic effects of leptin. Mice were instrumented with telemetry probes for measurement of blood pressure and heart rate and with venous catheters for intravenous infusions. After a 5-day control period, mice received leptin infusion (2 μg/kg per minute) for 7 days. Compared with control IRS2(flox/flox) mice, IRS2/POMC-cre mice had similar body weight and food intake (33±1 versus 35±1 g and 3.6±0.5 versus 3.8±0.2 g per day) but higher mean arterial pressure (MAP) and heart rate (110±2 versus 102±2 mm Hg and 641±9 versus 616±5 bpm). IRS2/Nestin-cre mice were heavier (38±2 g), slightly hyperphagic (4.5±1.0 g per day), and had higher MAP and heart rate (108±2 mm Hg and 659±9 bpm) compared with control mice. Leptin infusion gradually increased MAP despite decreasing food intake by 31% in IRS2(flox/flox) and in Nestin-cre control mice. In contrast, leptin infusion did not change MAP in IRS2/Nestin-cre or IRS2/POMC-cre mice. The anorexic and antidiabetic effects of leptin, however, were similar in all 3 groups. These results indicate that IRS2 signaling in the central nervous system, and particularly in POMC neurons, is essential for the chronic actions of leptin to raise MAP but not for its anorexic or antidiabetic effects.

Indexed as

AnimalsAppetiteBlood GlucoseBlood PressureDisease Models, AnimalEnergy MetabolismHypertensionInsulin Receptor Substrate ProteinsLeptinMaleMiceMice, TransgenicNeuronsPro-OpiomelanocortinSignal TransductionBlood GlucoseInsulin Receptor Substrate ProteinsIrs2 protein, mouseLeptinPro-Opiomelanocortinblood pressureheart rateinsulinobesityproopiomelanocortin

Identifiers

PMID26628674
PMCPMC4763950
OpenAlexW2188953028

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.