ArticleMolecular metabolism2026
Phosphomannomutase 1 restrains adipose thermogenic programming via inosine signaling.
Article in Molecular metabolism, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPhosphomannomutase 1 (PMM1) is an evolutionarily conserved metabolic enzyme classically linked to mannose metabolism, but its physiological role in adipose tissue remains unknown. This study aimed to define the function of PMM1 in thermogenic regulation and systemic metabolism.
methodsAn unbiased, integrative transcriptomic analysis of human subcutaneous adipose tissue was performed to relate PMM1 expression to clinical measures. Functional studies in mice and in primary murine and human adipocytes with PMM1 loss- and gain-of-function were conducted to investigate PMM1's role in the thermogenic program, assessed by metabolic phenotyping, RNA sequencing, targeted metabolomics, and signaling assays.
resultsPMM1 expression was inversely associated with obesity-related anthropometric and biochemical measures and was markedly induced by thermogenic stimulation. Adipocyte-specific Pmm1 knockdown promoted adipose thermogenic remodeling, increased energy expenditure, and protected mice from diet-induced obesity and insulin resistance. Mechanistically, PMM1 deficiency rerouted glucose metabolism into the pentose phosphate pathway, increasing inosine monophosphate and extracellular inosine. The elevated inosine engaged adenosine A
conclusionsPMM1 functions as a key metabolic brake on the adipose thermogenic program by limiting inosine production and downstream A
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.