Evidence map›Paper›PMID 30857366›Full record

ArticleNutrients2019

The PYY/Y2R-Deficient Mouse Responds Normally to High-Fat Diet and Gastric Bypass Surgery.

Brandon Boland, Michael B Mumphrey, Zheng Hao, Benji Gill, R Leigh Townsend, Sangho Yu, Heike Münzberg, Christopher D Morrison, James L Trevaskis, Hans-Rudolf Berthoud

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. The role of the gut-brain axis in bariatric surgery.Current opinion in neurobiology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

10 authors at 1 institution in 1 country.

Brandon BolandCardiovascular, Renal & Metabolic Diseases, MedImmune, Gaithersburg, MD 20878, USA. bolandb@MedImmune.com.
Michael B MumphreyNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. mumphrey@umich.edu.
Zheng HaoNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. haozhg@outlook.com.
Benji GillCardiovascular, Renal & Metabolic Diseases, MedImmune, Gaithersburg, MD 20878, USA. Gillb@MedImmune.com.
R Leigh TownsendNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. townserl@pbrc.edu.
Sangho YuNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. sangho.yu@pbrc.edu.ORCID 0000-0002-2973-7562
Heike MünzbergNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. heike.munzberg@pbrc.edu.
Christopher D MorrisonNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. christopher.morrison@pbrc.edu.
James L TrevaskisCardiovascular, Renal & Metabolic Diseases, MedImmune, Gaithersburg, MD 20878, USA. jimmytrevaskis@gmail.com.
Hans-Rudolf BerthoudNeurobiology of Nutrition & Metabolism Department, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. berthohr@pbrc.edu.
Pennington Biomedical Research Center · US

Funding

University of Michigan Training Program in Genomic ScienceT32HG000040 · NHGRI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Sebastian Zoellner · 1995 to 2026
$16.4M
Neural mechanisms controlling food intake and body weight after bariatric surgeryR01DK047348 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI BERTHOUD, HANS-RUDOLF · 1994 to 2018
$5.0M
FGF21 is an endocrine signal of protein restrictionR01DK105032 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI MORRISON, CHRISTOPHER D · 2016 to 2019
$1.4M
NHGRI NIH HHS T32 HG000040NIDDK NIH HHS R01 DK047348NIDDK NIH HHS R01 DK105032NIH HHS DK047348
6 · The paper itself

Abstract

background/goalsThe gut hormone peptide YY (PYY) secreted from intestinal L-cells has been implicated in the mechanisms of satiation via Y2-receptor (Y2R) signaling in the brain and periphery and is a major candidate for mediating the beneficial effects of bariatric surgery on appetite and body weight.

methodsHere we assessed the role of Y2R signaling in the response to low- and high-fat diets and its role in the effects of Roux-en-Y gastric bypass (RYGB) surgery on body weight, body composition, food intake, energy expenditure and glucose handling, in global Y2R-deficient (Y2RKO) and wildtype (WT) mice made obese on high-fat diet.

resultsBoth male and female Y2RKO mice responded normally to low- and high-fat diet in terms of body weight, body composition, fasting levels of glucose and insulin, as well as glucose and insulin tolerance for up to 30 weeks of age. Contrary to expectations, obese Y2RKO mice also responded similarly to RYGB compared to WT mice for up to 20 weeks after surgery, with initial hypophagia, sustained body weight loss, and significant improvements in fasting insulin, glucose tolerance, insulin resistance (HOMA-IR), and liver weight compared to sham-operated mice. Furthermore, non-surgical Y2RKO mice weight-matched to RYGB showed the same improvements in glycemic control as Y2RKO mice with RYGB that were similar to WT mice.

conclusionsPYY signaling through Y2R is not required for the normal appetite-suppressing and body weight-lowering effects of RYGB in this global knockout mouse model. Potential compensatory adaptations of PYY signaling through other receptor subtypes or other gut satiety hormones such as glucagon-like peptide-1 (GLP-1) remain to be investigated.

Indexed as

Gastric BypassAnimalsDiet, High-FatMaleMiceMice, KnockoutObesityPeptide YYReceptors, Gastrointestinal HormonePeptide YYpeptide YY receptorReceptors, Gastrointestinal Hormonebody compositionbody weightdiabetesenergy expenditureglucose toleranceincretininsulin toleranceobesity

Identifiers

PMID30857366
PMCPMC6471341
OpenAlexW2922466138

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.