Scholarlink

<p>Obesity reflects a chronic imbalance between energy intake and expenditure, accompanied by metabolic inflammation and ectopic lipid deposition. Accumulating evidence indicates that gut microbiota dysbiosis reshapes host nutrient handling and endocrine-immune signaling, with downstream consequences for thermogenic adipose tissues. Brown adipose tissue (BAT) supports energy dissipation via UCP1-dependent adaptive thermogenesis; however, in obesity, BAT often undergoes “whitening,” a maladaptive transition characterized by lipid accumulation, mitochondrial dysfunction, and reduced thermogenic capacity. This review synthesizes mechanistic and translational evidence linking obesity-associated microbiota alterations to BAT dysfunction through integrated gut-adipose and gut-liver communication. We discuss how microbially derived metabolites (including short-chain fatty acids and secondary bile acids), endotoxin-driven inflammation, and bile acid receptor signaling (FXR/TGR5) may converge on sympathetic tone, mitochondrial biogenesis, and lipid flux to favor BAT whitening. We further evaluate nutrition- and lifestyle-based strategies (dietary fiber and polyphenols, exercise, pre/pro/postbiotics, and bile acid-targeted approaches) that modulate microbial ecology and metabolic outputs, with potential to preserve BAT thermogenic identity and improve metabolic health. Clarifying the causal pathways and clinically actionable microbial signatures within this gut-adipose-liver network may inform future nutrition-oriented interventions for obesity and related metabolic disorders.</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

Gut microbiota, brown adipose tissue whitening, and obesity: nutritional modulators and metabolic crosstalk

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月16日

查看全文
  • Majid Ghodraty,
  • Mehrshad Fekri,
  • Maedeh Kiani,
  • Sepehr Esmaeel Zadegan,
  • Shailin Abdoli Rezaei,
  • Seyedeh Sara Mousavi Gilani,
  • Mahsa Manafi Varkiani,
  • Atie Ghafouri,
  • Nariman Mehrnia,
  • Masume Amudi,
  • Zahra Khodayar,
  • Amir Jouya Talaei,
  • Mohammad Baadkoubehazaveh

摘要

Obesity reflects a chronic imbalance between energy intake and expenditure, accompanied by metabolic inflammation and ectopic lipid deposition. Accumulating evidence indicates that gut microbiota dysbiosis reshapes host nutrient handling and endocrine-immune signaling, with downstream consequences for thermogenic adipose tissues. Brown adipose tissue (BAT) supports energy dissipation via UCP1-dependent adaptive thermogenesis; however, in obesity, BAT often undergoes “whitening,” a maladaptive transition characterized by lipid accumulation, mitochondrial dysfunction, and reduced thermogenic capacity. This review synthesizes mechanistic and translational evidence linking obesity-associated microbiota alterations to BAT dysfunction through integrated gut-adipose and gut-liver communication. We discuss how microbially derived metabolites (including short-chain fatty acids and secondary bile acids), endotoxin-driven inflammation, and bile acid receptor signaling (FXR/TGR5) may converge on sympathetic tone, mitochondrial biogenesis, and lipid flux to favor BAT whitening. We further evaluate nutrition- and lifestyle-based strategies (dietary fiber and polyphenols, exercise, pre/pro/postbiotics, and bile acid-targeted approaches) that modulate microbial ecology and metabolic outputs, with potential to preserve BAT thermogenic identity and improve metabolic health. Clarifying the causal pathways and clinically actionable microbial signatures within this gut-adipose-liver network may inform future nutrition-oriented interventions for obesity and related metabolic disorders.