Thermogenesis and Energy Metabolism in Brown Adipose Tissue in Animals Experiencing Cold Stress
Zhang X., Xiao J., Jiang M., Phillips CJC., Shi B.
Narrative Review, published in Int J Mol Sci (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Int J Mol Sci (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40244078
- PMCID
- PMC11989373
- DOI
- 10.3390/ijms26073233
- Citations
- 10
Abstract (original English)
Cold exposure is a regulatory biological functions in animals. The interaction of thermogenesis and energy metabolism in brown adipose tissue (BAT) is important for metabolic regulation in cold stress. Brown adipocytes (BAs) produce uncoupling protein 1 (UCP1) in mitochondria, activating non-shivering thermogenesis (NST) by uncoupling fuel combustion from ATP production in response to cold stimuli. To elucidate the mechanisms underlying thermogenesis and energy metabolism in BAT under cold stress, we explored how cold exposure triggers the activation of BAT thermogenesis and regulates overall energy metabolism. First, we briefly outline the precursor composition and function of BA. Second, we explore the roles of the cAMP- protein kinase A (PKA) and adenosine monophosphate-activated protein kinase (AMPK) signaling pathways in thermogenesis and energy metabolism in BA during cold stress. Then, we analyze the mechanism by which BA regulates mitochondria homeostasis and energy balance during cold stress. This research reveals potential therapeutic targets, such as PKA, AMPK, UCP1 and PGC-1α, which can be used to develop innovative strategies for treating metabolic diseases. Furthermore, it provides theoretical support for optimizing cold stress response strategies, including the pharmacological activation of BAT and the genetic modulation of thermogenic pathways, to improve energy
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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