Evidence map›Paper›PMID 34638990›Full record

ArticleInternational journal of molecular sciences2021

TNFSF14-Derived Molecules as a Novel Treatment for Obesity and Type 2 Diabetes.

Mark Agostino, Jennifer Rooney, Lakshini Herat, Jennifer Matthews, Allyson Simonds, Susan E Northfield, Denham Hopper, Markus P Schlaich, Vance B Matthews

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

9 authors at 4 institutions in 1 country.

Mark AgostinoCurtin Medical School, Curtin University, Bentley, WA 6102, Australia.ORCID 0000-0002-1799-0392
Jennifer RooneyDobney Hypertension Centre, School of Biomedical Sciences-Royal Perth Hospital Unit, University of Western Australia, Perth, WA 6009, Australia.
Lakshini HeratDobney Hypertension Centre, School of Biomedical Sciences-Royal Perth Hospital Unit, University of Western Australia, Perth, WA 6009, Australia.
Jennifer MatthewsDobney Hypertension Centre, School of Biomedical Sciences-Royal Perth Hospital Unit, University of Western Australia, Perth, WA 6009, Australia.
Allyson SimondsCurtin Medical School, Curtin University, Bentley, WA 6102, Australia.
Susan E NorthfieldDepartment of Biochemistry and Pharmacology, School of Biomedical Sciences, The University of Melbourne, Parkville, VIC 3010, Australia.ORCID 0000-0001-5619-9563
Denham HopperDepartment of Biochemistry and Pharmacology, School of Biomedical Sciences, The University of Melbourne, Parkville, VIC 3010, Australia.ORCID 0000-0002-0231-5220
Markus P SchlaichDepartment of Cardiology, Royal Perth Hospital, Perth, WA 6000, Australia.
Vance B MatthewsDobney Hypertension Centre, School of Biomedical Sciences-Royal Perth Hospital Unit, University of Western Australia, Perth, WA 6009, Australia.ORCID 0000-0001-9804-9344
The University of Western Australia · AUCurtin University · AUThe University of Melbourne · AURoyal Perth Hospital · AU

Funding

Diabetes Research WA VMDRWA2019
6 · The paper itself

Abstract

Obesity is one of the most prevalent metabolic diseases in the Western world and correlates directly with glucose intolerance and insulin resistance, often culminating in Type 2 Diabetes (T2D). Importantly, our team has recently shown that the TNF superfamily (TNFSF) member protein, TNFSF14, has been reported to protect against high fat diet induced obesity and pre-diabetes. We hypothesized that mimics of TNFSF14 may therefore be valuable as anti-diabetic agents. In this study, we use in silico approaches to identify key regions of TNFSF14 responsible for binding to the Herpes virus entry mediator and Lymphotoxin β receptor. In vitro evaluation of a selection of optimised peptides identified six potentially therapeutic TNFSF14 peptides. We report that these peptides increased insulin and fatty acid oxidation signalling in skeletal muscle cells. We then selected one of these promising peptides to determine the efficacy to promote metabolic benefits in vivo. Importantly, the TNFSF14 peptide 7 reduced high fat diet-induced glucose intolerance, insulin resistance and hyperinsulinemia in a mouse model of obesity. In addition, we highlight that the TNFSF14 peptide 7 resulted in a marked reduction in liver steatosis and a concomitant increase in phospho-AMPK signalling. We conclude that TNFSF14-derived molecules positively regulate glucose homeostasis and lipid metabolism and may therefore open a completely novel therapeutic pathway for treating obesity and T2D.

Indexed as

AnimalsBinding SitesBlood GlucoseComputer SimulationDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalGlucose IntoleranceHomeostasisHyperinsulinismHypoglycemic AgentsInsulin ResistanceLymphotoxin beta ReceptorMaleMiceMice, Inbred C57BLBlood GlucoseHypoglycemic AgentsLtbr protein, mouseLymphotoxin beta ReceptorPeptidesReceptors, Tumor Necrosis Factor, Member 14Tnfrsf14 protein, mouseTnfsf14 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 14LIGHTmetabolic syndromeobesitytherapyTNFSF14Type 2 Diabetes

Identifiers

PMID34638990
PMCPMC8508965
OpenAlexW3204462910

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.