Evidence map›Paper›PMID 38705901›Full record

ArticleEuropean journal of nutrition2024

Lactobacillus acidophilus KBL409 protects against kidney injury via improving mitochondrial function with chronic kidney disease.

Jimin Park, Ki Heon Nam, Bo Young Nam, Gyuri Kim, Hyoungnae Kim, Ki Uk Lee, Seok Cheon Song, Tae-Wook Nam, Woon-Ki Kim, Jung Tak Park and 4 more

Erratum issuedAbstract read
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In one paragraph

Article in European journal of nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Review
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Jimin Park *Department of Internal Medicine, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical Science, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
Ki Heon Nam *Division of Integrated Medicine, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Bo Young NamDepartment of Internal Medicine, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical Science, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
Gyuri KimDepartment of Internal Medicine, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical Science, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
Hyoungnae KimDivision of Nephrology, Soonchunhyang University Seoul Hospital, Seoul, Korea.
Ki Uk LeeKoBiolabs, Inc., Seoul, Korea.
Seok Cheon SongKoBiolabs, Inc., Seoul, Korea.
Tae-Wook NamKoBiolabs, Inc., Seoul, Korea.
Woon-Ki KimDepartment of Environmental Health Sciences, Graduate School of Public Health, Seoul National University, Seoul, Korea.
Jung Tak ParkDepartment of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
Tae-Hyun YooDepartment of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
Shin-Wook KangDepartment of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea.
GwangPyo KoKoBiolabs, Inc., Seoul, Korea.
Seung Hyeok HanDepartment of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea. hansh@yuhs.ac.ORCID http://orcid.org/0000-0001-7923-5635

Funding

Yonsei University College of Medicine 6-2021-0220
6 · The paper itself

Abstract

purposeRecent advances have led to greater recognition of the role of mitochondrial dysfunction in the pathogenesis of chronic kidney disease (CKD). There has been evidence that CKD is also associated with dysbiosis. Here, we aimed to evaluate whether probiotic supplements can have protective effects against kidney injury via improving mitochondrial function.

methodsAn animal model of CKD was induced by feeding C57BL/6 mice a diet containing 0.2% adenine. KBL409, a strain of Lactobacillus acidophilus, was administered via oral gavage at a dose of 1 × 10

resultsIn CKD mice, PGC-1α and AMPK, key mitochondrial energy metabolism regulators, were down-regulated. In addition, mitochondrial dynamics shifted toward fission, the number of fragmented cristae increased, and mitochondrial mass decreased. These alterations were restored by KBL409 administration. KBL409 supplementation also improved defects in fatty acid oxidation and glycolysis and restored the suppressed enzyme levels involved in TCA cycle. Accordingly, there was a concomitant improvement in mitochondrial respiration and ATP production assessed by mitochondrial function assay. These favorable effects of KBL409 on mitochondria ultimately decreased kidney fibrosis in CKD mice. In vitro analyses with butyrate recapitulated the findings of animal study.

conclusionsThis study demonstrates that administration of the probiotic Lactobacillus acidophilus KBL409 protects against kidney injury via improving mitochondrial function.

Indexed as

Disease Models, AnimalLactobacillus acidophilusMice, Inbred C57BLMitochondriaProbioticsRenal Insufficiency, ChronicAnimalsKidneyMaleMiceChronic kidney diseaseDysbiosisKBL409MitochondriaProbiotics

Identifiers

PMID38705901

What OpenQuestion holds

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Registered trials

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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.