ReviewCurrent obesity reports2026
Fueling or Fighting Cancer? The Thermogenic Paradox of Brown Adipose Tissue.
Review in Current obesity reports, 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
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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
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewThe global rise in obesity and metabolic syndrome has intensified interest in brown adipose tissue (BAT) as a regulator of energy metabolism and potential modulator of cancer risk. BAT-mediated thermogenesis and the browning of white adipose tissue (WAT) confer metabolic benefits that may reduce oncogenic susceptibility. However, emerging evidence reveals a paradoxical role for BAT in cancer progression, where tumor-induced thermogenic activation contributes to cancer-associated cachexia (CAC). This review article examines the cellular, molecular, and translational dimensions of this “thermogenic paradox”. RECENT
findingsA narrative synthesis was performed using literature from 2000 to 2025 retrieved from PubMed, Scopus, Web of Science, and Google Scholar. Peer-reviewed studies examining the molecular, genetic, and metabolic mechanisms linking BAT or adipose browning to carcinogenesis, obesity-related cancers, and CAC were included. Thematic integration emphasized regulatory pathways, endocrine signaling, and therapeutic implications. Adaptive browning, regulated by transcriptional drivers such as PRDM16, PPARγ, and PGC1-α, mitigates metabolic inflammation, enhances insulin sensitivity, and may exert tumor-suppressive effects. In contrast, tumor-secreted factors including parathyroid hormone-related protein (PTHrP) and interleukin-6 aberrantly induce uncoupling protein 1 (UCP1) expression and β3-adrenergic signaling, driving lipolysis and energy wasting in CAC. The dualistic effects of BAT underscore its context-dependent influence on cancer biology. BAT exemplifies a metabolic continuum between protection and pathology. Clarifying its regulatory mechanisms may inform precision therapies and integrated metabolic-oncology interventions, particularly relevant to low- and middle-income countries facing the double burden of obesity and cachexia.
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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 Socratic graph.