Evidence map›Paper›PMID 36107617›Full record

ArticleJCI insight2022

β Cell mass expansion during puberty involves serotonin signaling and determines glucose homeostasis in adulthood.

Anne-Laure Castell, Clara Goubault, Mélanie Ethier, Grace Fergusson, Caroline Tremblay, Marie Baltz, Dorothée Dal Soglio, Julien Ghislain, Vincent Poitout

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

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  17. Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2023
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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

9 authors at 2 institutions in 1 country.

Anne-Laure CastellMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Clara GoubaultMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Mélanie EthierMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Grace FergussonMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Caroline TremblayMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Marie BaltzMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Dorothée Dal SoglioCHU Sainte-Justine, Montreal, Quebec, Canada.
Julien GhislainMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Vincent PoitoutMontreal Diabetes Research Center, Centre de recherche du centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada.
Centre Hospitalier de l’Université de Montréal · CACentre Hospitalier Universitaire Sainte-Justine · CA

Funding

Neutral lipid dysregulation of the pancreatic beta-cellR01DK058096 · NIDDK · UNIVERSITY OF MONTREAL HOSPITAL · PI POITOUT, VINCENT · 2001 to 2020
$3.9M
NIDDK NIH HHS R01 DK058096
6 · The paper itself

Abstract

Puberty is associated with transient insulin resistance that normally recedes at the end of puberty; however, in overweight children, insulin resistance persists, leading to an increased risk of type 2 diabetes. The mechanisms whereby pancreatic β cells adapt to pubertal insulin resistance, and how they are affected by the metabolic status, have not been investigated. Here, we show that puberty is associated with a transient increase in β cell proliferation in rats and humans of both sexes. In rats, β cell proliferation correlated with a rise in growth hormone (GH) levels. Serum from pubertal rats and humans promoted β cell proliferation, suggesting the implication of a circulating factor. In pubertal rat islets, expression of genes of the GH/serotonin (5-hydroxytryptamine [5-HT]) pathway underwent changes consistent with a proliferative effect. Inhibition of the pro-proliferative 5-HT receptor isoform HTR2B blocked the increase in β cell proliferation in pubertal islets ex vivo and in vivo. Peripubertal metabolic stress blunted β cell proliferation during puberty and led to altered glucose homeostasis later in life. This study identifies a role of GH/GH receptor/5-HT/HTR2B signaling in the control of β cell mass expansion during puberty and identifies a mechanistic link between pubertal obesity and the risk of developing type 2 diabetes.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceAdultAnimalsCell ProliferationChildFemaleGlucoseHomeostasisHumansMaleRatsSerotoninSexual MaturationGlucoseSerotoninBeta cellsEndocrinologyMetabolism

Identifiers

PMID36107617
PMCPMC9675460
OpenAlexW4295898267

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.