Evidence map›Paper›PMID 27528227›Full record

ArticleOncotarget2016

Butyrate alleviates high fat diet-induced obesity through activation of adiponectin-mediated pathway and stimulation of mitochondrial function in the skeletal muscle of mice.

Jian Hong, Yimin Jia, Shifeng Pan, Longfei Jia, Huifang Li, Zhenqiang Han, Demin Cai, Ruqian Zhao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 227 citations in OpenAlex.

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  10. [Research progress in mechanisms of dietary resistant starch for regulating glucose and lipid metabolism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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68 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

8 authors at 2 institutions in 1 country.

Jian HongKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Yimin JiaKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Shifeng PanKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Longfei JiaKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Huifang LiKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Zhenqiang HanKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Demin CaiKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Ruqian ZhaoKey Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing, P. R. China.
Nanjing Agricultural University · CNYancheng Teachers University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dietary supplementation of butyrate can prevent diet-induced obesity through increasing mitochondrial function in mice, yet the up-stream signaling pathway remains elusive. In this study, weaned mice were divided into two groups, fed control (CON) and high-fat diet (HF, 45% energy from fat), respectively, for 8 weeks. HF-induced obese mice, maintained on HF diet, were then divided into two groups; HFB group was gavaged with 80 mg sodium butyrate (SB) per mice every other day for 10 days, while the HF group received vehicle. It was shown that five gavage doses of SB significantly alleviated HF diet-induced obesity and restored plasma glucose, insulin and leptin to control levels. Muscle contents of ADP and AMP were significantly increased, which was associated with enhanced mitochondrial oxidative phosphorylation and up-regulated expression of fatty acid oxidation enzymes and uncoupling proteins, UCP2 and UCP3 in the skeletal muscle. SB significantly enhanced the expression of adiponectin receptors (adipoR1/2) and AMP kinase (AMPK), while diminished the expression of histone deacetylase 1 (HDAC1). Higher H3K9Ac, a gene activation histone mark, was detected on the promoter of Adipor1/2, Ucp2 and Ucp3 genes that were activated in the muscle of SB-treated obese mice. Our results indicate that short-term oral administration of SB can alleviate diet-induced obesity and insulin resistance in mice through activation of adiponectin-mediated pathway and stimulation of mitochondrial function in the skeletal muscle.

Indexed as

AdiponectinAnimalsBlood GlucoseButyratesDiet, High-FatHistone Deacetylase 1HumansInsulinInsulin ResistanceLeptinLipid MetabolismMaleMiceMice, Inbred C57BLMice, ObeseMitochondriaAdiponectinAdipoq protein, mouseBlood GlucoseButyratesHdac1 protein, mouseHistone Deacetylase 1InsulinLeptinReceptors, AdiponectinUcp2 protein, mouseUcp3 protein, mouseUncoupling Protein 2Uncoupling Protein 3adipoR1adipoR2mitochondria functionobesityPathology Sectionsodium butyrate

Identifiers

PMID27528227
PMCPMC5302897
OpenAlexW2508309531

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.