Evidence map›Paper›PMID 25339680›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2014

Shp2 signaling in POMC neurons is important for leptin's actions on blood pressure, energy balance, and glucose regulation.

Jussara M do Carmo, Alexandre A da Silva, Sabira E Ebaady, Price O Sessums, Ralph S Abraham, Joel K Elmquist, Bradford B Lowell, John E Hall

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. 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
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Role of SOCS3 in POMC neurons in metabolic and cardiovascular regulation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  17. Article
  18. Article
  19. Role of PTP1B in POMC neurons during chronic high-fat diet: sex differences in regulation of liver lipids and glucose tolerance.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Jussara M do CarmoDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi; jdocarmo@umc.edu.
Alexandre A da SilvaDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi;
Sabira E EbaadyDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi;
Price O SessumsDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi;
Ralph S AbrahamDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi;
Joel K ElmquistDepartment of Pharmacology and Division of Hypothalamic Research, Department of Internal Medicine, Utah Southwestern Medical Center, Dallas, Texas; and.
Bradford B LowellDivision of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
John E HallDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, and Cardiovascular-Renal Research Center, University of Mississippi Medical Center, Jackson, Mississippi;
University of Mississippi Medical Center · USBeth Israel Deaconess Medical Center · USThe University of Texas Southwestern 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 P01HL-51971NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P20GM104357
6 · The paper itself

Abstract

Previous studies showed that Src homology-2 tyrosine phosphatase (Shp2) is an important regulator of body weight. In this study, we examined the impact of Shp2 deficiency specifically in proopiomelanocortin (POMC) neurons on metabolic and cardiovascular function and on chronic blood pressure (BP) and metabolic responses to leptin. Mice with Shp2 deleted in POMC neurons (Shp2/Pomc-cre) and control mice (Shp2(flox/flox)) were implanted with telemetry probes and venous catheters for measurement of mean arterial pressure (MAP) and leptin infusion. After at least 5 days of stable control measurements, mice received leptin infusion (2 μg·kg(-1)·day(-1) iv) for 7 days. Compared with Shp2(flox/flox) controls, Shp2/Pomc-cre mice at 22 wk of age were slightly heavier (34 ± 1 vs. 31 ± 1 g) but consumed a similar amount of food (3.9 ± 0.3 vs. 3.8 ± 0.2 g/day). Leptin infusion reduced food intake in Shp2(flox/flox) mice (2.6 ± 0.5 g) and Shp2/Pomc-cre mice (3.2 ± 0.3 g). Despite decreasing food intake, leptin infusion increased MAP in control mice, whereas no significant change in MAP was observed in Shp2/Pomc-cre mice. Leptin infusion also decreased plasma glucose and insulin levels in controls (12 ± 1 to 6 ± 1 μU/ml and 142 ± 12 to 81 ± 8 mg/100 ml) but not in Shp2/Pomc-cre mice. Leptin increased V̇o2 by 16 ± 2% in controls and 7 ± 1% in Shp2/Pomc-cre mice. These results indicate that Shp2 signaling in POMC neurons contributes to the long-term BP and antidiabetic actions of leptin and may play a modest role in normal regulation of body weight.

Indexed as

AnimalsArterial PressureBlood GlucoseBody WeightBrainEatingEnergy MetabolismHomeostasisInfusions, IntravenousInsulinLeptinMaleMice, 129 StrainMice, Inbred C57BLMice, KnockoutMotor ActivityBlood GlucoseInsulinLeptinPro-OpiomelanocortinProtein Tyrosine Phosphatase, Non-Receptor Type 11Ptpn11 protein, mouseacute stressblood pressureenergy balanceglucose regulationheart rate

Identifiers

PMID25339680
PMCPMC4269667
OpenAlexW2066037847

What OpenQuestion holds

Textmetadata
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.