ArticleThe Journal of clinical investigation2022
Is thermogenesis really needed for brown adipose tissue-mediated metabolic benefit?
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Brown Adipose Tissue: Molecular Mechanisms of Regulation, Physiological Functions, and Therapeutic Targets.MedComm · 2026Review
- Global loss of selenocysteine lyase in mice drives lipid accumulation in brown adipocytes.American journal of physiology. Endocrinology and metabolism · 2026Article
- Activation of brown adipose tissue by a low-protein diet ameliorates hyperglycemia in a diabetic lipodystrophy mouse model.Scientific reports · 2023Article
- Activation of brown adipose tissue by a low-protein diet ameliorates hyperglycemia in a diabetic lipodystrophy mouse model.Research square · 2023Article
- Selenium and selenoproteins in thermogenic adipocytes.Archives of biochemistry and biophysics · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Brown adipose tissue (BAT) dissipates energy in the form of heat and functions as a metabolic sink for lipids, glucose, and branched-chain amino acids. Enhanced BAT thermogenesis is thought to tightly couple with beneficial energy metabolism. However, in this issue of the JCI, Huang et al. report a mouse model in which BAT thermogenesis was impaired, yet systemic glucose and lipid homeostasis were improved, on a high-fat diet compared with what occurred in control mice. The authors showed that BAT-specific deletion of mitochondrial thioredoxin-2 (TRX2) impaired adaptive thermogenesis through elevated mitochondrial reactive oxygen species (ROS) and cytosolic efflux of mitochondrial DNA. On the other hand, TRX2 loss enhanced lipid uptake in the BAT and protected mice from obesity, hypertriglyceridemia, and insulin resistance. This study provides a unique model in which BAT does not require thermogenesis per se to function as a lipid sink that leads to metabolic benefits in vivo.
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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 OpenQuestion graph.