Evidence map›Paper›PMID 28973869›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Butyrylcholinesterase gene transfer in obese mice prevents postdieting body weight rebound by suppressing ghrelin signaling.

Vicky Ping Chen, Yang Gao, Liyi Geng, Stephen Brimijoin

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. LEAP2 changes with body mass and food intake in humans and mice.The Journal of clinical investigation · 2019
    Trial
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  4. Review
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  7. Observational
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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

4 authors at 1 institution in 1 country.

Vicky Ping ChenDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905 chen.vicky@mayo.edu brimijoin@mayo.edu.
Yang GaoDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905.
Liyi GengDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905.
Stephen BrimijoinDepartment of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905 chen.vicky@mayo.edu brimijoin@mayo.edu.
Mayo Clinic · US

Funding

Cocaine hydrolase gene therapy for cocaine abuse (DPI)DP1DA031340 · NIDA · MAYO CLINIC ROCHESTER · PI BRIMIJOIN, WILLIAM STEPHEN · 2010 to 2014
$3.9M
Definitive Preclinical Studies of Hydrolase Gene Transfer to Treat Cocaine AbuseUH3DA042492 · NIDA · MAYO CLINIC ROCHESTER · PI HOOTEN, W. MICHAEL, PENG, KAH-WHYE · 2019 to 2021
$3.1M
Definitive Preclinical Studies of Hydrolase Gene Transfer to Treat Cocaine AbuseUG3DA042492 · NIDA · MAYO CLINIC ROCHESTER · PI BRIMIJOIN, WILLIAM STEPHEN, PENG, KAH-WHYE · 2016 to 2017
$2.8M
NIDA NIH HHS DP1 DA031340NIDA NIH HHS UG3 DA042492NIDA NIH HHS UH3 DA042492
6 · The paper itself

Abstract

The worldwide prevalence of obesity is increasing at an alarming rate but treatment options remain limited. Despite initial success, weight loss by calorie restriction (CR) often fails because of rebound weight gain. Postdieting hyperphagia along with altered hypothalamic neuro-architecture appears to be one direct cause of this undesirable outcome. In response to calorie deficiency the circulating levels of the appetite-promoting hormone, acyl-ghrelin, rise sharply. We hypothesize that proper modulation of acyl-ghrelin and its receptor's sensitivity will favorably impact energy intake and reprogram the body weight set point. Here we applied viral gene transfer of the acyl-ghrelin hydrolyzing enzyme, butyrylcholinesterase (BChE), in a mouse model of diet-induced obesity. Our results confirmed that BChE overexpression decreased circulating acyl-ghrelin levels, suppressed CR-provoked ghrelin signaling, and restored central ghrelin sensitivity. In addition to maintaining healthy body weights, BChE treated mice had modest postdieting food intake and showed normal glucose homeostasis. Spontaneous activity and energy expenditure did not differ significantly between treated and untreated mice after body weight rebound, suggesting that BChE gene transfer did not alter energy expenditure in the long term. These findings indicate that combining BChE treatment with CR could be an effective approach in treating human obesity and aiding lifelong weight management.

Indexed as

Caloric RestrictionAnimalsAppetiteBody WeightButyrylcholinesteraseEatingGhrelinHyperphagiaMaleMiceMice, ObeseObesitySignal TransductionWeight GainWeight LossButyrylcholinesteraseGhrelinbody weight reboundbutyrylcholinesterasediet-induced obesityfood intakeghrelin

Identifiers

PMID28973869
PMCPMC5642694
OpenAlexW2758723125

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.