Evidence map›Paper›PMID 24928195›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Intestinal deletion of leptin signaling alters activity of nutrient transporters and delayed the onset of obesity in mice.

Annabelle Tavernier, Jean-Baptiste Cavin, Maude Le Gall, Robert Ducroc, Raphaël G P Denis, Françoise Cluzeaud, Sandra Guilmeau, Yassine Sakar, Laurence Barbot, Nathalie Kapel and 5 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Regulation of intestinal growth in response to variations in energy supply and demand.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2018
    Review
  7. Association between polymorphisms inDiabetes, metabolic syndrome and obesity : targets and therapy · 2018
    Article
  8. Review
  9. Regulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2 diabetic mice.Laboratory investigation; a journal of technical methods and pathology · 2016
    Article
  10. Sodium-glucose cotransport.Current opinion in nephrology and hypertension · 2015
    Review
  11. 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

15 authors at 6 institutions in 3 countries.

Annabelle TavernierInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Jean-Baptiste CavinInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Maude Le GallInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Robert DucrocInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Raphaël G P DenisUniversité Paris Diderot, Sorbonne Paris Cité, Unité de Biologie Fonctionnelle et Adaptative, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 8251, Paris, France;
Françoise CluzeaudInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Sandra GuilmeauInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Yassine SakarInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France;
Laurence BarbotService de Coprologie Fonctionnelle, Hopital La Pitié Salpêtrière, Paris, France;
Nathalie KapelService de Coprologie Fonctionnelle, Hopital La Pitié Salpêtrière, Paris, France;
Johanne Le BeyecInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France; Université Pierre et Marie Curie, Paris, France;
Francisca JolyInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France; Service de Gastroenterologie et d'Assistance Nutritive, Hopital Beaujon, Clichy, France; and.
Streamson ChuaDepartment of Medicine and Neuroscience, Albert Einstein College of Medicine, New York, New York, USA.
Serge LuquetUniversité Paris Diderot, Sorbonne Paris Cité, Unité de Biologie Fonctionnelle et Adaptative, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 8251, Paris, France;
Andre BadoInstitut National de la Santé et de la Recherche Médicale (INSERM) Unité Mixte de Recherche en Santé (UMRS) 1149, Unité de Formation et de Recherche (UFR) de Médecine Paris Diderot, Sorbonne Paris Cite, Paris, France; andre.bado@inserm.fr.
Inserm · FRSorbonne Université · FRAlbert Einstein College of Medicine · USCentre National pour la Recherche Scientifique et Technique (CNRST) · MADélégation Paris 7 · FRSorbonne Paris Cité · FR

Funding

RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
NIDDK NIH HHS P30 DK026687NIDDK NIH HHS P30-DK-026687
6 · The paper itself

Abstract

The importance of B-isoform of leptin receptor (LEPR-B) signaling in the hypothalamus, pancreas, or liver has been well characterized, but in the intestine, a unique site of entry for dietary nutrition into the body, it has been relatively ignored. To address this question, we characterized a mouse model deficient for LEPR-B specifically in intestinal epithelial cells (IECs). (IEC)LEPR-B-knockout (KO) and wild-type (WT) mice were generated by Cre-Lox strategy and fed a normal or high-fat diet (HFD). The analyses of the animals involved histology and immunohistochemistry of intestinal mucosa, indirect calorimetric measurements, whole-body composition, and expression and activities of nutrient transporters. (IEC)LEPR-B-KO mice exhibited a 2-fold increase in length of jejunal villi and have normal growth on a normal diet but were less susceptible (P<0.01) to HFD-induced obesity. No differences occurred in energy intake and expenditure between (IEC)LEPR-B-WT and -KO mice, but (IEC)LEPR-B-KO mice fed an HFD showed increased excreted fats (P<0.05). Activities of the Na(+)/glucose cotransporter SGLT-1 and GLUT2 were unaffected in LEPR-B-KO jejunum, while GLUT5-mediated fructose transport and PepT1-mediated peptide transport were substantially reduced (P<0.01). These data demonstrate that intestinal LEPR-B signaling is important for the onset of diet-induced obesity. They suggest that intestinal LEPR-B could be a potential per os target for prevention against obesity.

Indexed as

AnimalsBlotting, WesternBody CompositionBody WeightCell ProliferationCells, CulturedDiet, High-FatEnergy IntakeFemaleGlucose Transporter Type 2Glucose Transporter Type 5Glucose Transport Proteins, FacilitativeImmunoenzyme TechniquesIntestinal MucosaLeptinMaleGlucose Transporter Type 2Glucose Transporter Type 5Glucose Transport Proteins, FacilitativeLeptinleptin receptor, mousePeptide Transporter 1Receptors, LeptinRNA, MessengerSlc15a1 protein, mouseSlc2a2 protein, mouseSlc2a5 protein, mouseSymportersabsorptionenergy expendituregut mucosahigh-fat diethypothalamic neuropeptides

Identifiers

PMID24928195
PMCPMC4139897
OpenAlexW2005972439

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.