Evidence map›Paper›PMID 29617867›Full record

ArticleJournal of animal science2018

Weaning disrupts intestinal antioxidant status, impairs intestinal barrier and mitochondrial function, and triggers mitophagy in piglets.

S T Cao, C C Wang, H Wu, Q H Zhang, L F Jiao, C H Hu

Abstract read
In one paragraph

Article in Journal of animal science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

72 citing papers in PubMed, 102 citations in OpenAlex.

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  20. Review

12 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 1 institution in 1 country.

S T CaoAnimal Science College, Zhejiang University, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Hangzhou, China.
C C WangAnimal Science College, Zhejiang University, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Hangzhou, China.
H WuAnimal Science College, Zhejiang University, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Hangzhou, China.
Q H ZhangAnimal Science College, Zhejiang University, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Hangzhou, China.
L F JiaoAnimal Science College, Zhejiang University, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Hangzhou, China.
C H HuAnimal Science College, Zhejiang University, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, Hangzhou, China.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study, we investigated the influence of weaning on antioxidant status, intestinal integrity, mitochondrial function, and the mitophagy level in piglets (weaned at 21 d) during the 1 wk after weaning. The redox status was measured by antioxidant enzymes activities, related genes expression, and malondialdehyde (MDA) content in jejunum. The intestinal barrier function was assessed by the Ussing chamber and expression of tight junction proteins in the jejunum. The function of intestine mitochondria was measured by mitochondrial DNA (mtDNA) content and activities of mitochondria oxidative phosphorylation complexes. The levels of light chain 3-1 (LC3-I), light chain 3-II (LC3-II), PTEN-induced putative kinase 1 (PINK1), and Parkin were determined to investigate whether mitophagy is involved in the weaning process. The results showed that, as compared with the preweaning phase (d 0), weaning suppressed (P < 0.05) the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) on d 3 and d 7 postweaning, decreased (P < 0.05) the expression of copper and zinc superoxide dismutase (Cu/Zn-SOD), manganese-containing superoxide dismutase (Mn-SOD) on d 3 postweaning, declined (P < 0.05) the level of glutathione peroxidase 1 (GPX-1) and glutathione peroxidase 4 (GPX-4) on d 3 and d 7 postweaning, and increased (P < 0.05) MDA content in jejunum on d 3 and d 7 postweaning. The jejunal transepithelial electrical resistance and levels of occludin, claudin-1, and zonula occludens-1 on d 3 and d 7 postweaning were reduced (P < 0.05), and paracellular flux of fluorescein isothiocyanatedextran (4 kDa) on d 3 and d 7 postweaning was increased (P < 0.05). Weaning induced mitochondrial dysfunction, as demonstrated by decreased (P < 0.05) content of mtDNA on d 3 and d 7 postweaning and declined (P < 0.05) activities of mitochondria complexes (I, II, III, IV) in jejunum on d 1, d 3, and d 7 postweaning. Weaning led to an increased (P < 0.05) expression level of mitophagy-related proteins, PINK1 and Parkin, in the intestinal mitochondria, as well as an enhancement (P < 0.05) of the ratio of LC3-II to LC3-I content in the jejunal mucosa on d 1, d 3, and d 7 postweaning. These results suggest that weaning disrupted intestinal oxidative balance, and this imbalance may impair intestinal barrier and mitochondrial function and trigger mitophagy in piglets.

Indexed as

MitophagyAnimalsAntioxidantsFemaleGlutathione PeroxidaseIntestinal MucosaJejunumMaleMalondialdehydeMitochondriaOxidation-ReductionOxidative StressSuperoxide DismutaseSwineTight Junction ProteinsWeaningAntioxidantsGlutathione PeroxidaseMalondialdehydeSuperoxide DismutaseTight Junction Proteins

Identifiers

PMID29617867
PMCPMC6093500
OpenAlexW2795511476

What OpenQuestion holds

Textmetadata
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.