ArticleCell death & disease2026
CD300e modulates metabolic programs in adipose tissue macrophages during obesity.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies in monozygotic twins discordant for body mass index (BMI) revealed that individuals with obesity exhibit elevated expression of the immune receptor CD300e in white adipose tissue (WAT). Notably, CD300e levels decreased following weight loss, implicating its involvement in adipose tissue remodeling and metabolic regulation. To elucidate the functional role of CD300e, we employed a Cd300e knockout (Cd300e-/-) mouse model subjected to a high-fat diet (HFD). Our findings demonstrate that CD300e deficiency exacerbates obesity-associated metabolic dysfunction, including increased weight gain, adipocyte hypertrophy, hepatic steatosis, and impaired glucose and insulin sensitivity. Adipose tissue macrophages (ATMs) lacking CD300e displayed reduced lipid and glucose uptake, alongside diminished mitochondrial respiration-a phenotype consistent with a broader metabolic impairment, as evidenced by proteomic profiling. These metabolic deficits were genotype-dependent and persisted after 16 weeks of HFD. Concurrently, adipocytes from Cd300e-/- mice exhibited enhanced lipogenesis and attenuated lipolysis. Remarkably, the impaired metabolic fitness exhibited by Cd300e-/- mouse macrophages was recapitulated in human cells upon gene silencing. Collectively, these results establish CD300e as essential for ATM metabolic activation, positioning it as a key regulator of adipose tissue homeostasis and a critical mediator of obesity-induced metabolic dysfunction. Given its pivotal role, CD300e emerges as a promising therapeutic target for modulating adipose tissue function and improving metabolic health in obesity.
Indexed as
Identifiers
What 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.