Evidence map›Paper›PMID 39987092›Full record

ArticleBMC veterinary research2025

Camel milk exosomes regulate glucose metabolism by inhibiting mitochondrial complex I in hepatocytes.

Bin Yang, Shifeng Du, Ling Liu, Jingjing Wang, Demtu Er

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

5 authors.

Bin Yang *Inner Mongolia Key Laboratory of Basic Veterinary Science, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010011, China.
Shifeng Du *Inner Mongolia Key Laboratory of Basic Veterinary Science, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010011, China.
Ling LiuInner Mongolia Key Laboratory of Basic Veterinary Science, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010011, China.
Jingjing WangInner Mongolia Key Laboratory of Basic Veterinary Science, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010011, China.
Demtu ErInner Mongolia Key Laboratory of Basic Veterinary Science, College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot, 010011, China. eedmt@imau.edu.cn.

Funding

Discipline Project of College of Veterinary Medicine, Inner Mongolia Agricultural University SYKJYB202304Natural Science Foundation Project of Inner Mongolia Autonomous Region 2023LHMS03054Plan (Science and Technology Cooperation) Project of 2023 Autonomous Region Major Research and Development and Achievements Transformation, Science and Technology Agency of Inner Mongolia Autonomous Region 2023KJHZ0003Program for improving the Scientific Reasearch Ability of Youth Teachers of Inner Mongolia Agricultural University BR230157
6 · The paper itself

Abstract

backgroundCamel milk is known to have hypoglycemic properties. Previous studies found that camel milk exosomes (CM-exo) may regulate cellular glucose metabolism through the inhibition of mitochondrial complex I, but this hypothesis has not been verified by other experiments. The objective of this study was to verify the hypothesis that CM-exo regulated glucose metabolism in hepatocytes by inhibiting mitochondrial complex I pathway. AML12 cells were treated with extracted exosomes from camel milk and the effect of the CM-exo on cell viability was examined by cell counting kit (CCK)-8 assays. The glucose content of the cell culture medium was measured to determine the glucose consumption of the cells. Lactate release from the cells was determined by measuring the lactate content in the cell culture medium. The glycogen content of AML12 cells was detected. The activity of complex I and the contents of ATP, NAD

resultsThe results of this study showed that a high dose of CM-exo inhibited the viability of AML12 cells. It promoted glucose consumption, glycogen content and lactate release in AML12 cells, inhibited complex I activity, ATP content, NAD

conclusionsBy inhibiting the activity of mitochondrial complex I in hepatocytes, CM-exo inhibited oxidative phosphorylation, oxidation of NADH to NAD

Indexed as

CamelusElectron Transport Complex IExosomesGlucoseHepatocytesMilkAnimalsCell LineCell SurvivalMiceElectron Transport Complex IGlucoseAML12 cellsCamel milk exosomesComplex IGluconeogenesis

Identifiers

PMID39987092
PMCPMC11846279

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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.