Evidence map›Paper›PMID 28664920›Full record

ReviewNature reviews. Endocrinology2017

FGF1 - a new weapon to control type 2 diabetes mellitus.

Emanuel Gasser, Christopher P Moutos, Michael Downes, Ronald M Evans

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

63 citing papers in PubMed, 107 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  6. Human FGF1Cells · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. FGF1 as a New Promising Therapeutic Target in Type 2 Diabetes: Advances in Research and Clinical Trials.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

3 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

4 authors at 1 institution in 1 country.

Emanuel GasserGene Expression Laboratory, Salk Institute for Biological Studies.
Christopher P MoutosGene Expression Laboratory, Salk Institute for Biological Studies.
Michael DownesGene Expression Laboratory, Salk Institute for Biological Studies.
Ronald M EvansGene Expression Laboratory, Salk Institute for Biological Studies.
Salk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Reuben Shaw · 1985 to 2026
$82.8M
Yeast Genetics and Stress Response Genes-BiomedicalP42ES010337 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TUKEY, ROBERT H · 2000 to 2022
$69.8M
Transcriptional GenomicsP01HL088093 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WITZTUM, JOSEPH L. · 2008 to 2018
$26.4M
HORMONAL REGULATION OF MAMMALIAN GENE EXPRESSIONR37DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2000 to 2019
$16.0M
Spatial Regulation of Developmental Gene ExpressionR01HL105278 · NHLBI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2011 to 2019
$4.0M
Hormonal Regulation of Mammalian Gene ExpressionR01DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2021 to 2024
$2.6M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA014195NHLBI NIH HHS P01 HL088093NHLBI NIH HHS R01 HL105278NIDDK NIH HHS R01 DK057978NIDDK NIH HHS R37 DK057978NIEHS NIH HHS P42 ES010337
6 · The paper itself

Abstract

A hypercaloric diet combined with a sedentary lifestyle is a major risk factor for the development of insulin resistance, type 2 diabetes mellitus (T2DM) and associated comorbidities. Standard treatment for T2DM begins with lifestyle modification, and includes oral medications and insulin therapy to compensate for progressive β-cell failure. However, current pharmaceutical options for T2DM are limited in that they do not maintain stable, durable glucose control without the need for treatment intensification. Furthermore, each medication is associated with adverse effects, which range from hypoglycaemia to weight gain or bone loss. Unexpectedly, fibroblast growth factor 1 (FGF1) and its low mitogenic variants have emerged as potentially safe candidates for restoring euglycaemia, without causing overt adverse effects. In particular, a single peripheral injection of FGF1 can lower glucose to normal levels within hours, without the risk of hypoglycaemia. Similarly, a single intracerebroventricular injection of FGF1 can induce long-lasting remission of the diabetic phenotype. This Review discusses potential mechanisms by which centrally administered FGF1 improves central glucose-sensing and peripheral glucose uptake in a sustained manner. Specifically, we explore the potential crosstalk between FGF1 and glucose-sensing neuronal circuits, hypothalamic neural stem cells and synaptic plasticity. Finally, we highlight therapeutic considerations of FGF1 and compare its metabolic actions with FGF15 (rodents), FGF19 (humans) and FGF21.

Indexed as

Insulin ResistanceAnimalsBlood GlucoseDiabetes Mellitus, Type 2Disease Models, AnimalFemaleFibroblast Growth Factor 1Follow-Up StudiesHumansInsulinMaleMice, Inbred C57BLRandom AllocationRoleTreatment OutcomeBlood GlucoseFibroblast Growth Factor 1Insulin

Identifiers

PMID28664920
PMCPMC5839646
OpenAlexW2728295845

What OpenQuestion holds

Textmetadata
LicenceTDM
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.