Evidence map›Paper›PMID 24813890›Full record

ArticleCell reports2014

Hypothalamic agouti-related peptide neurons and the central melanocortin system are crucial mediators of leptin's antidiabetic actions.

Gabriel H M Gonçalves, Wenjing Li, Adriana V C-G Garcia, Mariana S Figueiredo, Christian Bjørbæk

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025
    Review
  3. Article
  4. History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Leptin signaling and leptin resistance.Medical review (2021) · 2022
    Review
  9. Article
  10. PMInnovation (Cambridge (Mass.)) · 2022
    Article
  11. Review
  12. The acromegaly lipodystrophy.Frontiers in endocrinology · 2022
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Gabriel H M GonçalvesDepartment of Medicine, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Wenjing LiDepartment of Medicine, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Adriana V C-G GarciaDepartment of Medicine, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Mariana S FigueiredoDepartment of Medicine, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Christian BjørbækDepartment of Medicine, Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. Electronic address: cbjorbae@bidmc.harvard.edu.
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
Regulation of Hypothalamic Proopiomelanocortin by LeptinR01DK060673 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BJORBAEK, CHRISTIAN · 2002 to 2010
$2.5M
Leptin Signaling in Hypothalamic Neurons and Glutamate ReceptorsR01DK094040 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KIM, YOUNG-BUM · 2012 to 2015
$1.5M
NIDDK NIH HHS DK060673NIDDK NIH HHS DK094040NIDDK NIH HHS P30 DK046200NIDDK NIH HHS R01 DK060673NIDDK NIH HHS R01 DK094040
6 · The paper itself

Abstract

Leptin has beneficial effects on glucose metabolism via actions in the hypothalamus, but the roles of specific subgroups of neurons responsible for these antidiabetic effects remain unresolved. We generated diabetic Lep(ob/ob) or Lepr(db/db) mice lacking or re-expressing leptin receptors (LepRb) in subgroups of neurons to explore their contributions to leptin's glucose-lowering actions. We show that agouti-related peptide (AgRP)-expressing neurons are both required and sufficient to correct hyperglycemia by leptin. LepRb in pro-opiomelanocortin (POMC) neurons or steroidogenic factor-1 (SF1) neurons are not required. Furthermore, normalization of blood glucose by leptin is blunted in Lep(ob/ob)/MC4R-null mice, but not in Lep(ob/ob) mice lacking neuropeptide Y (NPY) or gamma-aminobutyric acid (GABA) in AgRP neurons. Leptin's ability to improve glucose balance is accompanied by a reduction in circulating glucagon. We conclude that AgRP neurons play a crucial role in glucose-lowering actions by leptin and that this requires the melanocortin system, but not NPY and GABA.

Indexed as

Agouti-Related ProteinAnimalsBlood GlucoseDiabetes Mellitus, ExperimentalFemaleGlucagonHumansHypothalamusLeptinMaleMelanocortinsMiceMice, TransgenicNeuronsReceptors, LeptinAgouti-Related ProteinBlood GlucoseGlucagonLeptinMelanocortinsReceptors, Leptin

Identifiers

PMID24813890
PMCPMC4369586
OpenAlexW1965190353

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.