Evidence map›Paper›PMID 20581837›Full record

ArticleNature medicine2010

Serotonin regulates pancreatic beta cell mass during pregnancy.

Hail Kim, Yukiko Toyofuku, Francis C Lynn, Eric Chak, Toyoyoshi Uchida, Hiroki Mizukami, Yoshio Fujitani, Ryuzo Kawamori, Takeshi Miyatsuka, Yasuhiro Kosaka and 9 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Nature medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 326 papers.

0numbers the graph read from it
0cells of the map it votes in
326citing papers in PubMed
28.8field-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

326 citing papers in PubMed, 578 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Article
  6. CD168 Identifies Proliferating Pancreatic Islet Cells in Murine and Human.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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266 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 4 institutions in 3 countries.

Hail KimDiabetes Center, University of California-San Francisco, San Francisco, California, USA.
Yukiko Toyofuku
Francis C Lynn
Eric Chak
Toyoyoshi Uchida
Hiroki Mizukami
Yoshio Fujitani
Ryuzo Kawamori
Takeshi Miyatsuka
Yasuhiro Kosaka
Katherine Yang
Gerard Honig
Marieke van der Hart
Nina Kishimoto
Juehu Wang
Soroku Yagihashi
Laurence H Tecott
Hirotaka Watada
Michael S German
University of California, San Francisco · USJuntendo University · JPHirosaki University · JPUniversity of British Columbia · CA

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2003 to 2019
$21.8M
Molecular Control of Pancreatic Islet DevelopmentU19DK061245 · NIDDK · UNIVERSITY OF CHICAGO · PI GERMAN, MICHAEL S · 2001 to 2005
$5.9M
DIFFERENTIATION IN THE ENDOCRINE AND EXOCRINE PANCREASR01DK021344 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 1986 to 2014
$3.4M
NIDDK NIH HHS P30 DK063720NIDDK NIH HHS R01 DK021344NIDDK NIH HHS U19 DK061245
6 · The paper itself

Abstract

During pregnancy, the energy requirements of the fetus impose changes in maternal metabolism. Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, whereas prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing beta cells. However, the exact mechanisms by which the lactogenic hormones drive beta cell expansion remain uncertain. Here we show that serotonin acts downstream of lactogen signaling to stimulate beta cell proliferation. Expression of serotonin synthetic enzyme tryptophan hydroxylase-1 (Tph1) and serotonin production rose sharply in beta cells during pregnancy or after treatment with lactogens in vitro. Inhibition of serotonin synthesis by dietary tryptophan restriction or Tph inhibition blocked beta cell expansion and induced glucose intolerance in pregnant mice without affecting insulin sensitivity. Expression of the G alpha(q)-linked serotonin receptor 5-hydroxytryptamine receptor-2b (Htr2b) in maternal islets increased during pregnancy and normalized just before parturition, whereas expression of the G alpha(i)-linked receptor Htr1d increased at the end of pregnancy and postpartum. Blocking Htr2b signaling in pregnant mice also blocked beta cell expansion and caused glucose intolerance. These studies reveal an integrated signaling pathway linking beta cell mass to anticipated insulin need during pregnancy. Modulators of this pathway, including medications and diet, may affect the risk of gestational diabetes.

Indexed as

Pregnancy, AnimalAnimalsFemaleGene Expression ProfilingGlucoseInsulinInsulin-Secreting CellsIslets of LangerhansMiceMice, Inbred C57BLPlacental LactogenPregnancyProlactinSerotoninTryptophan HydroxylaseGlucoseInsulinPlacental LactogenProlactinSerotoninTPH1 protein, humanTph1 protein, mouseTPH2 protein, humanTph2 protein, mouseTryptophan Hydroxylase

Identifiers

PMID20581837
PMCPMC2921604
OpenAlexW2051567027

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.