Evidence map›Paper›PMID 10022436›Full record

ArticleThe Journal of clinical endocrinology and metabolism1999

Leptin suppression of insulin secretion and gene expression in human pancreatic islets: implications for the development of adipogenic diabetes mellitus.

J Seufert, T J Kieffer, C A Leech, G G Holz, W Moritz, C Ricordi, J F Habener

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
15.3field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 278 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Pancreatic Exocrine Insufficiency Is Surprisingly Common.Integrative medicine (Encinitas, Calif.) · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Leptin signaling and leptin resistance.Medical review (2021) · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Activation of Cx43 Hemichannels Induces the Generation of CaInternational journal of molecular sciences · 2021
    Article
  20. Role of Leptin in the Digestive System.Frontiers in pharmacology · 2021
    Review

16 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 1 country.

J SeufertLaboratory of Molecular Endocrinology, Massachusetts General Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston 02114, USA.
T J Kieffer
C A Leech
G G Holz
W Moritz
C Ricordi
J F Habener
Massachusetts General Hospital · USHarvard University · USNew York University · USUniversity of Miami · US

Funding

Insulinotropin: A Modulator Of B-Cell Glucose SignalingR01DK045817 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI HOLZ, GEORGE G · 2001 to 2008
$3.0M
GLUCAGON BIOSYNTHESIS &METABOLISMR01DK030834 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI HABENER, JOEL F · 1986 to 2008
$1.9M
NIDDK NIH HHS DK30834NIDDK NIH HHS R01 DK030834NIDDK NIH HHS R01 DK045817
6 · The paper itself

Abstract

Previously we demonstrated the expression of the long form of the leptin receptor in rodent pancreatic beta-cells and an inhibition of insulin secretion by leptin via activation of ATP-sensitive potassium channels. Here we examine pancreatic islets isolated from pancreata of human donors for their responses to leptin. The presence of leptin receptors on islet beta-cells was demonstrated by double fluorescence confocal microscopy after binding of a fluorescent derivative of human leptin (Cy3-leptin). Leptin (6.25 nM) suppressed insulin secretion of normal islets by 20% at 5.6 mM glucose. Intracellular calcium responses to 16.7 mM glucose were rapidly reduced by leptin. Proinsulin messenger ribonucleic acid expression in islets was inhibited by leptin at 11.1 mM, but not at 5.6 mM glucose. Leptin also reduced proinsulin messenger ribonucleic acid levels that were increased in islets by treatment with 10 nM glucagon-like peptide-1 in the presence of either 5.6 or 11.1 mM glucose. These findings demonstrate direct suppressive effects of leptin on insulin-producing beta-cells in human islets at the levels of both stimulus-secretion coupling and gene expression. The findings also further indicate the existence of an adipoinsular axis in humans in which insulin stimulates leptin production in adipocytes and leptin inhibits the production of insulin in beta-cells. We suggest that dysregulation of the adipoinsular axis in obese individuals due to defective leptin reception by beta-cells may result in chronic hyperinsulinemia and may contribute to the pathogenesis of adipogenic diabetes.

Indexed as

ObesityReceptors, Cell SurfaceCalciumCarrier ProteinsCells, CulturedDiabetes MellitusGene ExpressionGlucagonGlucagon-Like Peptide 1GlucoseHumansInsulinInsulin SecretionIslets of LangerhansLeptinPeptide FragmentsCalciumCarrier ProteinsGlucagonGlucagon-Like Peptide 1GlucoseInsulinLEPR protein, humanLeptinPeptide FragmentsPotassium ChannelsProinsulinProtein PrecursorsProteinsReceptors, Cell SurfaceReceptors, LeptinRNA, Messenger

Identifiers

PMID10022436
PMCPMC2927866
OpenAlexW2028843279

What OpenQuestion holds

Texttitle and abstract
measurements read1
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.