ArticleInternational journal of obesity (2005)2025
Phosphatidylethanolamine/PKA signal axis mediated human milk extracellular vesicles enhance adipose thermogenesis and lipolysis via mitochondrial remodeling.
Article in International journal of obesity (2005), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Cross-Species Analysis of Milk Extracellular Vesicles Reveals a Conserved Innate Core and a Divergent, Human-Specific Adaptive Immune Fraction.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesEmerging evidence suggests that extracellular vesicles (EVs) in breast milk may serve as an abundant source of candidates for regulating metabolism. Our study aims to identify phospholipids derived from human milk EVs (mEVs) that can benefit people with obesity.
methodsInfant mice were either fed with formula milk or breastfed to investigate whether mEVs affect adipose tissue physiology in infants. Human milk samples were collected from nursing mothers who had given birth at Shanghai Tongren Hospital. UPLC-MS/MS was used to characterize lipidomic profile of human colostrum and mature milk. Body weight changes, H&E staining, blood lipid test, GTT and ITT test were measured to evaluate physiology changes of phospholipid administrated high-fat-diet (HFD) mice. Infrared measurement, western blot, qPCR and IHC analysis were measured to evaluate thermogenesis. RNA-seq and qPCR were used to evaluate the cluster of genes and pathways. Seahorse, electron microscope observation and qPCR were measured to evaluate mitochondrial remodeling of adipocyte. PKA inhibitor (H89) was used to evaluate signal axis of mitochondrial coupling respiration in adipocyte.
resultsLipidomic analyses of mEVs identified phosphatidylethanolamine (PE) as a signature molecule, whose abundance remains consistent between colostrum and mature milk. PE significantly enhanced brown adipocyte thermogenic respiration in vivo, activated mitochondrial biogenesis transcriptionally, and suppressed mitochondrial clearance. These results led to an increased number of mitochondria and promotes the beiging process. RNA sequencing revealed that PE potentially remodels mitochondria through the PKA signaling pathway, which may influence thermogenesis and lipolysis. The activation mechanism of PE in adipocytes was confirmed by a reduction in thermogenesis phenotype.
conclusionsmEVs-derived PE serves as a universal cellular adjustor, regulating mitochondrial efficiency via PE/PKA signaling in response to shifts in demand of energy. mEVs serve as a tool for mother-to-child signaling bridge, which maintain a long-time health of adipose tissue.
Indexed as
Identifiers
40847069What OpenQuestion holds
Registered trials
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.