Scholarlink

Purpose of Review <p>The 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”.</p> Recent Findings <p>A 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.</p> Summary <p>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.</p> Graphical Abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Fueling or Fighting Cancer? The Thermogenic Paradox of Brown Adipose Tissue

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月18日

查看全文
  • Jonathan Jaime G. Guerrero,
  • Paolo C. Encarnacion,
  • Chih-Hao Wang,
  • Mark Angelo S. del Rosario,
  • Kin Israel Notarte,
  • Jiayan Zhou,
  • Yi-Ta Hsieh,
  • Wan-Yu Wang,
  • Ching-Wen Chang,
  • Wan-Chun Li

摘要

Purpose of Review

The 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 Findings

A 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.

Summary

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.

Graphical Abstract