Evidence map›Paper›PMID 34381196›Full record

ReviewNature reviews. Endocrinology2021

GDF15: emerging biology and therapeutic applications for obesity and cardiometabolic disease.

Dongdong Wang, Emily A Day, Logan K Townsend, Djordje Djordjevic, Sebastian Beck Jørgensen, Gregory R Steinberg

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 313 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
313citing papers in PubMed, 3 pooled it
50.3field-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

313 citing papers in PubMed, 3 syntheses or guidelines pooled it, 473 citations in OpenAlex.

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  9. Effects of Individualized Step Targets on Physical Activity in COPD. A Randomized Study.International journal of chronic obstructive pulmonary disease · 2025
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253 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Dongdong WangCentre for Metabolism, Obesity and Diabetes Research and the Department of Medicine, McMaster University, Hamilton, ON, Canada.ORCID http://orcid.org/0000-0002-6195-4428
Emily A DayCentre for Metabolism, Obesity and Diabetes Research and the Department of Medicine, McMaster University, Hamilton, ON, Canada.ORCID http://orcid.org/0000-0003-3245-5715
Logan K TownsendCentre for Metabolism, Obesity and Diabetes Research and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
Djordje DjordjevicGlobal Obesity and Liver Disease Research, Novo Nordisk A/S, Maaloev, Denmark.ORCID http://orcid.org/0000-0003-3669-6292
Sebastian Beck JørgensenGlobal Obesity and Liver Disease Research, Novo Nordisk A/S, Maaloev, Denmark.ORCID http://orcid.org/0000-0002-9648-0971
Gregory R SteinbergCentre for Metabolism, Obesity and Diabetes Research and the Department of Medicine, McMaster University, Hamilton, ON, Canada. gsteinberg@mcmaster.ca.ORCID http://orcid.org/0000-0001-5425-8275
McMaster University · CANovo Nordisk (Denmark) · DKMcMaster University Medical Centre · CA

Funding

CIHR 201709FDN-CEBA-116200
6 · The paper itself

Abstract

Growth differentiation factor 15 (GDF15) is a member of the TGFβ superfamily whose expression is increased in response to cellular stress and disease as well as by metformin. Elevations in GDF15 reduce food intake and body mass in animal models through binding to glial cell-derived neurotrophic factor family receptor alpha-like (GFRAL) and the recruitment of the receptor tyrosine kinase RET in the hindbrain. This effect is largely independent of other appetite-regulating hormones (for example, leptin, ghrelin or glucagon-like peptide 1). Consistent with an important role for the GDF15-GFRAL signalling axis, some human genetic studies support an interrelationship with human obesity. Furthermore, findings in both mice and humans have shown that metformin and exercise increase circulating levels of GDF15. GDF15 might also exert anti-inflammatory effects through mechanisms that are not fully understood. These unique and distinct mechanisms for suppressing food intake and inflammation makes GDF15 an appealing candidate to treat many metabolic diseases, including obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease, cardiovascular disease and cancer cachexia. Here, we review the mechanisms regulating GDF15 production and secretion, GDF15 signalling in different cell types, and how GDF15-targeted pharmaceutical approaches might be effective in the treatment of metabolic diseases.

Indexed as

Molecular Targeted TherapyAnimalsCardiovascular DiseasesDiabetes Mellitus, Type 2Growth Differentiation Factor 15HumansMetabolic DiseasesMetforminNon-alcoholic Fatty Liver DiseaseObesityGDF15 protein, humanGrowth Differentiation Factor 15Metformin

Identifiers

PMID34381196
OpenAlexW3193150046

What OpenQuestion holds

Texttitle and abstract
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.