Evidence map›Paper›PMID 33751819›Full record

ArticleJournal of cellular and molecular medicine2021

FGF19 protects skeletal muscle against obesity-induced muscle atrophy, metabolic derangement and abnormal irisin levels via the AMPK/SIRT-1/PGC-α pathway.

Ai Guo, Kai Li, Hong-Chuan Tian, Zhen Fan, Qiu-Nan Chen, Yun-Fei Yang, Jing Yu, Yong-Xin Wu, Qian Xiao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Ai GuoDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Kai LiDepartment of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hong-Chuan TianDepartment of Orthopedics, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Zhen FanDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qiu-Nan ChenDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yun-Fei YangDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jing YuDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yong-Xin WuDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qian XiaoDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID 0000-0001-8855-6561
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNDalian Medical University · CN

Funding

National Key Clinical Specialties Construction Program of China (2013) 544National Natural Science Foundation of China 81701382National Natural Science Foundation of China 81801385
6 · The paper itself

Abstract

Obesity is associated with biological dysfunction in skeletal muscle. As a condition of obesity accompanied by muscle mass loss and physical dysfunction, sarcopenic obesity (SO) has become a novel public health problem. Human fibroblast growth factor 19 (FGF19) plays a therapeutic role in metabolic diseases. However, the protective effects of FGF19 on skeletal muscle in obesity and SO are still not completely understood. Our results showed that FGF19 administration improved muscle loss and grip strength in young and aged mice fed a high-fat diet (HFD). Increases in muscle atrophy markers (FOXO-3, Atrogin-1, MuRF-1) were abrogated by FGF19 in palmitic acid (PA)-treated C2C12 myotubes and in the skeletal muscle of HFD-fed mice. FGF19 not only reduced HFD-induced body weight gain, excessive lipid accumulation and hyperlipidaemia but also promoted energy expenditure (PGC-1α, UCP-1, PPAR-γ) in brown adipose tissue (BAT). FGF19 treatment restored PA- and HFD-induced hyperglycaemia, impaired glucose tolerance and insulin resistance (IRS-1, GLUT-4) and mitigated the PA- and HFD-induced decrease in FNDC-5/irisin expression. However, these beneficial effects of FGF19 on skeletal muscle were abolished by inhibiting AMPK, SIRT-1 and PGC-1α expression. Taken together, this study suggests that FGF19 protects skeletal muscle against obesity-induced muscle atrophy, metabolic derangement and abnormal irisin secretion partially through the AMPK/SIRT-1/PGC-α signalling pathway, which might be a potential therapeutic target for obesity and SO.

Indexed as

Adipose Tissue, BrownAMP-Activated Protein KinasesAnimalsCell LineDiet, High-FatFibroblast Growth FactorsFibronectinsHyperglycemiaHyperlipidemiasInsulin ResistanceLipid MetabolismMaleMiceMice, Inbred C57BLMuscle Fibers, SkeletalMuscle, SkeletalAMP-Activated Protein KinasesFGF19 protein, humanFibroblast Growth FactorsFibronectinsFNDC5 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseSirtuin 1FGF19insulin resistanceirisinlipid accumulationmuscle atrophyobesitysarcopenic obesity

Identifiers

PMID33751819
PMCPMC8034456
OpenAlexW3135337295

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.